Diabetes

fitocosmetic

10 Coisas que Você Precisa Saber Sobre Diabetes

O diabetes se caracteriza pela deficiência de produção e/ou de ação da insulina. O diabetes tipo 1 é resultante da destruição autoimune das células produtoras de insulina. O diagnóstico desse tipo de diabetes acontece, em geral, durante a infância e a adolescência, mas pode também ocorrer em outras faixas etárias.

Já no diabetes tipo 2, o pâncreas produz insulina, mas há incapacidade de absorção das células musculares e adiposas. Esse tipo de diabetes é mais comum em pessoas com mais de 40 anos, acima do peso, sedentárias, sem hábitos saudáveis de alimentação.

1. No tratamento do diabetes, o ideal é que a glicose fique entre 70 e 100mg/dL.  A partir de 100mg/dL  em jejum ou 140mg/dL duas horas após as refeições, considera-se hiperglicemia e, abaixo de 70mg/dL,hipoglicemia. Se a glicose permanecer alta demais por muito tempo, haverá mais possibilidade de complicações de curto e longo prazo. A hipoglicemia pode causar sintomas indesejáveis e com complicações que merecem atenção.

Se o diabetes não for tratado de forma adequada, podem surgir complicações, como retinopatia,nefropatia, neuropatia, pé diabético, infarto do miocárdio, acidente vascular cerebral, entre outros.AVC

Se o paciente já estiver com diagnóstico de complicação crônica, há tratamentos específicos para ajudar a levar uma vida normal.

  • Níveis elevados de açúcar no sangue e glicação: A glicose é um combustível celular vital. No entanto, a exposição crónica de glicose pode afetar a idade do corpo por um processo chamado de glicação.
  •  A glicação pode ocorrer pela exposição crônica ao açúcar exógeno, nos alimentos, ou endógeno, como no caso do Diabetes.
  • A consequência principal desse processo é o estresse oxidativo celular, tendo como consequência, o envelhecimento precoce.
  • Obesidade e 33 enfermedades vinculadas com Diabetes

    A obesidade é caracterizada pelo acúmulo de gordura corporal e pode acarretar graves problemas de saúde e levar até àManchete_Obesidade morte. O Brasil tem cerca de 18 milhões de pessoas consideradas obesas. Somando o total de indivíduos acima do peso, o montante chega a 70 milhões, o dobro de há três décadas.

  • CHILE

La diabetes, también conocida como diabetes mellitus, es una afección crónica representada por un conjunto de trastornos metabólicos que perjudica a diversos órganos y tejidos, y que en la actualidad afecta a más del 7% de la población chilena -más de un millón 150 mil habitantes- según cifras del Ministerio de Salud.

 

De acuerdo a la Asociación de Diabéticos de Chile (Adich), este padecimiento se desarrolla cuando el páncreas no produce insulina, o bien, cuando el cuerpo no es capaz de emplear eficazmente la insulina que elabora. “Esto provoca hiperglicemia (un exceso de azúcar en la sangre), que daña considerablemente numerosos sistemas del organismo, especialmente el sistema vascular y el sistema nervioso”, indicaron.

En este sentido, desde la organización explicaron que existen dos categorías predominantes de diabetes: la de Tipo 1, que aqueja principalmente a niños y adolescentes y que se manifiesta por la necesidad de insulina para sobrevivir, y la de Tipo 2, que afecta al 99% de los diabéticos en Chile y que se caracteriza por la incapacidad de emplear de forma eficiente esta hormona.

Pese a que existen diversos métodos para tratar la diabetes, como regular la dieta con un especialista, dejar hábitos como el cigarrillo y consumir medicamentos recetados, también existen ciertos alimentos que permiten a los pacientes diabéticos controlar la enfermedad.

Así lo postularon una serie de expertos consignados por el portal estadounidense Univisión, los cuales explicaron cómo la cebolla, el té verde y el ginseng, entre otros, pueden ayudarte a mantener a raya la diabetes.  Fuente: BioBioChile

NZ

NEEM & diabetes mellitus  diezmos

 

Overview

With its extremely bitter properties, neem has been a cornerstone of Ayurveda therapy for pitas, or disorders caused by overeating sweets.

As the tale is told, when an Indian manufacturer applied for government of a neem capsule e to treat diabetes, it was approved in 24 hours.

After almost 4,500 years of almost continuous use, even the Indian equivalent of the FDA apparently believes that “anything from neem has to be good,” according to Robert Larson, one of the first Americans to recognize the value of neem.

Some of the earliest reports on neem, dating back to

A 1973 report in Medicine and Surgery

(Not available online)

Indicated that insulin requirements could be cut by up to 50 percent for

Patients who take five grams of neem leaf daily. Several other studies undertaken before the advent of the internet made data accessible confirm that report in humans.

More studies that are recent have focused on animals, primarily

Diabetic mice and rabbits.

One study http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10919098&query_hl=18&itool=pubmed_docsum

indicates that neem leaf had a hypoglycemic effect comparable to the prescription drug glibenclamide, and noted that neem might be beneficial in preventing or delaying the onset of the disease.

CAUTION

Insulin dependent diabetics must still monitor blood sugar levels carefully

when supplementing with neem.

Neem may cause significant increases in blood sugar levels and

continuing insulin at the same dose may result in hypoglycemia.

Recent Research

Indian J Physiol Pharmacol.

2006 Jul Sep;50(3):241

-.

Department of Pharmacology, Institute of Medical Sciences, Banaras Hindu University,

Varanasi 221 005.

http://www.ncbi.nlm.nih.gov/pubmed/17193895?ordinalpos=1&itool=EntrezSystem2.PEntrez.

Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Standardized aqueous extract of Neem (Azadirachta indica) leaves (AIE) has been diezmos

Scientists discover a natural molecule to treat type 2 diabetes

Friday, July 17, 2015 by: Dr.Sofiya

Learn more: http://www.naturalnews.com/050431_omega-3_type_2_diabetes_fatty_acids.html#ixzz3gH7mfQDS

(NaturalNews) Most people in the medical profession agree that the current approach towards diabetes treatment is simply not working. This is evidenced by the fact that the number of type 2 diabetics in the United States – and around the world – has been steadily growing in recent years. It is estimated that there are close to 30 million diabetics in America alone. Diabetes is a major challenge to the healthcare system, as it can lead to problems with the heart, kidneys, wound healing and vision, just to name a few. That is why the search is on to look for alternative treatment modalities and to find different approaches to diabetes remedies that will have a larger impact on the growing number of people who suffer from this disease. Read on to find out about one such alternative treatment.

New research out of Quebec

This latest research has been done at the Universite Laval in Quebec. There, scientists have discovered a special molecule, chemically related to fatty acids, that is able to imitate the effects that physical exercise has on the regulation of blood sugars. Researchers from the university teamed up with the Quebec Heart and Lung Center and the Institute of Nutrition and Function Foods to study this molecule more closely to try to understand more about the remarkable effects it can have on blood sugar control.

Research in context

Many researchers, while they found this latest discovery hopeful, were not entirely surprised by it. After all, the medical profession has known for years that there is a link between the dietary intake of omega-3 fatty acids and reduced insulin resistance. It is this reduced resistance that translates into better blood sugar control, which in turn can fend off some of the more serious complications of this disease.

What lead scientist Professor Andre Marette and his colleagues discovered was a bioactive lipid which is related to fatty acids in structure and which is called protectin D1. In the course of the study, it was found that this lipid, and others in the same family, were able to trigger the release of interleukin-6 in the muscle tissue. This is also the body’s response to exercise. An increase in interleukin-6 levels is important biologically as this chemical is able to help move glucose from the blood stream to the muscle cells and is also able to reduce hepatic production of glucose.

These effects were born out by laboratory research which found that higher levels of this lipid in the blood stream was linked to an improvement in the body’s response to and use of insulin, which translates directly into better overall glucose control.

In short, the scientists involved on this study hope to continue with this line of research in the future, and have actually filed for patent for this lipid with a goal of developing new treatments for type 2 diabetes that might lead to better disease management – and quality of life – for millions of diabetics around the globe.

Sources:

http://www.sciencedaily.com

http://www.diabetes.co.uk

http://www.fiercebiotechresearch.com

Learn more: http://www.naturalnews.com/050431_omega-3_type_2_diabetes_fatty_acids.html#ixzz3gH6z8wfv

Peru

Uso de Medicina Tradicional en Diabetes Mellitus No Insulino – dependiente

Freddy Valdivia, Marcos Hidalgo

Resumen

Objetivos: Determinar el uso de la Medicina Tradicional en los pacientes con Diabetes Mellitus No Insulino Dependiente (DMNID) en el Servicio de Endocrinología del Hospital Nacional Guillermo Almenara Irigoyen (HNGAI). Métodos: Evaluación por Encuesta de 102 pacientes durante los meses de Mayo y junio de 1996 en el Consultorio Externo del servicio de Endocrinología del HNGAI. Resultados: 68,6% de los pacientes utilizaron alguna Medicina Tradicional, sin diferencia entre los sexos, siendo las más utilizadas la Gentianella arborocea, la Uncaria sp, y la Cyclanthera pedata.
De estos pacientes, el 73% utilizó 2 ó más productos, y el 60% refirió efecto favorable. El uso de la Medicina Tradicional no se encontró asociado al tratamiento con dieta, tabletas o insulina. Conclusiones: es frecuente el uso de la Medicina Tradicional por el paciente con DMNID, siendo este uso desconocido por el médico, y aun cuando no se ha demostrado científicamente efecto favorable de estas medicinas, es que los pacientes hacen uso de una gran diversidad de ellos. Se hace necesario el estudio de estos productos, para demostrar su utilidad o no en el manejo del DMNID.

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1.- Ginseng.

El extracto de dicha especie aumentaría la sensibilidad a la insulina en pacientes con la enfermedad, aseguró el médico John L. Sievenpiper  Universidad de Toronto (Canadá). Esta hormona “suele ser menos efectiva en caso de diabetes, pero el ginseng ayuda a combatir esa condición provocando que los pacientes aprovechen mejor la insulina que tienen”, explicó el especialista.

2.- Canela.

Para controlar los niveles de azúcar en la sangre, y reducir la presión arterial en pacientes diabéticos, bastaría con consumir media chucharadita de esta especia diariamente. Así lo postuló el nutricionista estadounidense Richard Anderson, quien explicó que “Gracias a esto, la canela ayudaría a prevenir diversas complicaciones de la diabetes”.

3.- Melón amargo.

De acuerdo a lo explicado por Jiming Ye, especialista del Instituto de Materia Médica de Shanghái (China), el melón amargo tiene un efecto similar al del ejercicio: “ayuda a los diabéticos a aprovechar la glucosa y a mantenerla en niveles estables. Aunque hay muchas drogas que hacen eso, el melón amargo no tendría efectos secundarios ni riesgos”, indicó.

4.- Arándano azul.

Esta rica fruta permitiría evitar los problemas en los ojos que se vinculan a la diabetes. Según un estudio publicado por el Molecular Nutrition & Food Research, “Los antioxidantes contenidos en el arándano azul protegen los vasos capilares y los nervios de los ojos de los daños que pueden ocasionarles los altos niveles de azúcar en la sangre o la hipertensión”.5.- Gimnema.

De acuerdo a una investigación del King’s College de Londres (Reino Unido), esta planta de la India tiene un alto contenido de ácido gimnémico que ayuda a incrementar la producción de insulina, permitiendo un mejor control de los niveles de azúcar en la sangre.

6.- Té verde.

El té verde permitiría elevar la sensibilidad a la insulina y evitar los problemas cardiovasculares comunes en pacientes con diabetes, según indicó Hiroshi Tsuneki, integrante de la Universidad de Toyoma (Japón). “Lo ideal para obtener sus beneficios sería tomar entre 4 y 8 tazas de té al día” recomendó Tsuneki.

7.- Nopal.

En palabras de Alberto Frati, perteneciente al Colegio Mexicano de Medicina Interna, esta planta disminuiría los niveles de azúcar en la sangre y, además, ayudaría a mantenerlos estables. “El nopal contiene mucha fibra y otras sustancias que controlan y normalizan el metabolismo del azúcar, por lo que no debe faltar en la dieta de alguien con diabetes”, explicó el especialista.

8.- Wereke.

El wereke, también llamado guareque, es una planta muy efectiva para reducir y mantener los niveles de glucosa. Pero además, aporta propiedades antiinflamatorias y antioxidantes que permitirían evitar otras complicaciones vinculadas a la enfermedad, de acuerdo al médico de la Universidad Autónoma Metropolitana (México), Francisco Cruz Sosa.

9.- Cebolla.

Consumir al menos 100 gramos de cebolla morada cruda al día ayudaría a disminuir los niveles de glucosa en pacientes con diabetes 1 y 2, casi tanto como algunos medicamentos, según la investigación de una universidad en Sudán. Lo anterior, en parte se debería a que esta planta herbácea es rica en el elemento azufre y en metabolitos flavonoides.

10.- Omega 3.

Estos ácidos grasos -que se encuentran en los pescados azules, algunas semillas y las nueces, entre otros alimentos- elevarían la sensibilidad a la insulina en pacientes diabéticos, de modo que permitirían controlar los niveles de glucosa. De acuerdo a Andrew Odegaard, médico de la Universidad de Minnesota (EEUU), “Lo mejor es consumirlos a través de los alimentos, así se garantiza una mejor alimentación”.

Fuente: BioBioChile http://www.biobiochile.cl/2013/11/14/dia-mundial-de-la-diabetes-10-remedios-naturales-que-te-ayudaran-a-controlarla.shtml

Infusión de eucalipto

El eucalipto ha sido un remedio tradicional para la diabetes. Ponga 3 hojas tiernas de eucalipto en 1/2 litro de agua y lo hierve por cinco minutos. Tome tres tacitas al día alternando con unas tazas de canela.

No diabetes: A infusão feita com as folhas ajuda a reduzir a glicemia.  Recomenda-se não mais do que uma xícara de chá por dia, lembrando que isso não substitui o uso da insulina.

Fuente: BioBioChile http://www.biobiochile.cl

Por otra parte, las células del epitelio tubular sufren inhibición de la proliferación y apoptosis bajo un ambiente prolongado de concentraciones altas de glucosa, esto acompañado de un incremento del estrés oxidativo (Park y col., 2001; Allen y col., 2003; Verzola y col., 2004)

Para tomar en cuenta…

Cabe destacar que, de acuerdo a la Asociación Americana de Diabetes (ADA por sus siglas en inglés), es recomendable que antes de utilizar estos remedios naturales los pacientes conversen con su médico, pues algunas plantas y suplementos pueden tener efectos secundarios en algunos de ellos o bien interferir con el funcionamiento de otros medicamentos.

En este sentido, la ADA llama a los diabéticos a no dejar sus tratamientos convencionales y que, ante cualquier cambio que experimenten al agregar comidas en su dieta, se lo comenten a su especialista.

Debe recordarse que, como indicó la Adich, “el control médico regular y el compromiso del paciente con su tratamiento evita la aparición de complicaciones crónicas”, como la Neuropatía -compromiso de los nervios-, la Nefropatía -compromiso del riñón y deterioro vascular- y Retinopatía -compromiso de la retina-.

Lo anterior ya que, en su grado más grave, la diabetes puede llegar a ser invalidante y desencadenar ceguera, amputaciones, insuficiencia renal y daño cardiovascular.

Fuente: BioBioChile

Eucalyptus (cha)   escudo2

Instituto Venezolano de Investigaciones Cientificas (ICV)

Universidad Central Instituto de Zoologia , Medicna Experimental

Universidad Simon Rodriguez

Universidad Central Faculdad de Farmacia

Un tipo de cha que proviene de una formula de los indiginas ausralianos quienes usaban el arbol Eucaliptos para tratar enfermedades respiratorios y diabetes.El etnobotanico -investigador Giovani Rutilo modifica el formulario en Venezuela.

Las hojas de Eucalipto contienen…aceite essencial, canfenos, terpineol, carburos terpenicos, sesquiterpenicos, valerianicos, aldehidos butiricos, cetonas y taninis.

Durante las investigaciones observamos que la principal funcion de cha es disolver las grasas saturadas, que se alojan en las paredes de las venas, en las arterias, en los capillares, y en las celulas.

Las grasas saturadas son pastosas como la mantequilla. se quedan pegadas y la mas  grave es que son imperables.  El cha de Eucalipto preparado de un formulario unico normalice la glicemia.

TE RUTILO

We are experimenting with a natural product developed in Venezuela which may reduce blood sugar levels. It is a tea developed by a local scientist using the Eucalipto leaf based on a formula developed by indigeneous peoples in Australia.

¿Qué es Té Rutilo? 

El TÉ RUTILO es un producto 100% Natural, sin agregado de sustancias químicas de síntesis, el origen del te rutilo proviene de una formula Natural de los Indígenas australianos, que usaban el árbol de Eucaliptus para tratar las enfermedades COMO DIABETES, esta fórmula fue modificada durante las investigaciones realizadas durante muchos años, por el etnobotánico investigador Giovanni Rutilo.

Investigaciones 

Normalizador de las alteraciones de la Glicemia

Normaliza niveles de colesterol y triglicéridos

Excelente Adelgazante

Cada frasco contiene: eucaliptus globulus al 100%.

Cada 100 gramos de hojas modificadas deshidratadas, pulverizadas contienen un 1-3% de Eucaliptol

Modo de empleo: adulto: vierta una cucharadita tipo postre (3 gramos) en dos litros de agua, mézclese bien y deje reposar durante 10 horas, luego hervir hasta reducir a un litro.

El te rutilo es un producto 100% natural, sin agregados de sustancias químicas de síntesis. El origen del te rutilo proviene de una formula de los indígenas australianos, quienes usarban el árbol de eucalipto para tratar las enfermedades respiratorias, diabetes y otras.

Dicha formula fue modificada gracias a las investigaciones realizadas durante muchos años , por el etno- botánico investigador Giovanni Rutilo.

El árbol y las hojas de eucalipto contienen:

Aceites esencial (éter oxido terpénico), canfenos , terpineol; carburos terpénico ( alfapineno); alcoholes alifáticos y sesquiterpénicos (eudesmol); aldehídos butíricos, valeriánicos , caproicos y cetonas; taninos; sustancias desintoxicantes; pigmentos flavónicos (heterópsidos del quecetol); un herópsido fenólico complejo, caliptosido; acidos fenólicos (gallico icafeico); resinas un principio amargo; acidos valerianocos; ésteres de acido acético; sustancias saponinas; cineol; ésteres de acido fórmico; eugenol; esencia verde; menta; alcanfor y otras.

Estas sustancias fueron separadas y probadas, lo cual arrojó resultados notables para el tratamiento de muchas enfermedades. Asi lo revelan los pacientes quienes publican sus testimonios, todos los días domingos en la Revista Dominical encartada en el periódico Últimas Noticias de circulación nacional en Venezuela. Una de las sustancias modificadas es el Eucaliptol.

Las hojas de Eucaliptos tienen un 60% o 70% de Eucalipto, y se redujo entre 1% y 3%. Asi como el café le eliminan la cafeína, mediantes procesos naturales, se redujo el eucaliptol para la formula del Té Rutilo. De igual manera se modificaron otras sustancias. 

Durante las investigaciones observamos que la principal función del Té Rutilo es disolver las grasas saturadas que se alojan en las paredes de las venas, en las arterias, en los capilares y en las células. Las grasas saturadas son pastosas como la mantequilla, se quedan pegadas y lo mas grave que son impermeables, no dejan pasar la sangre. Si la sangre no pasa, no pasan los nutrientes, ni el oxigeno, no los medicamentos de esta manera se enferman las células se asfixian y se mueren de hambre, lo cual produce un porcentaje alto de enfermedades

Beneficios: 

Excelente para normalizar las alteraciones de la glicemia

Efectivo adelgazante

Ayuda a disolver los cálculos renales

Bueno para reumatismo crónico en general

Excelente para cicatrización de úlceras y várices

Excelente reductor de grasas en venas y arterias

Normaliza los niveles de colesterol y triglicéridos 

african mujer.abs

Como utilizar as folhas do Eucalipto:

Infusão: Para cada colher de sopa de folhas de eucalipto picadas use 300 ml de água. Coloque as folhas e a água para ferver por 2 minutos, retire do fogo, coe e adoce com mel. Para usá-las por causa de problemas nas vias respiratórias ou urinárias, deve-se beber de três a quatro xícaras de chá por dia.


Peru

El extracto acuoso de Taraxacum officinalis Weber “diente de león” por vía oral tiene efecto hipoglucemiante en ratonesalbinos de la cepa CF1.

Hipótesis Específicas: • Existe una dosis letal media (DL50) del exCastro et al (2002), estudiarón metabolitos secundarios de plantas medicinales con efecto hipoglucemiante donde determinaron el cromo como factor de tolerancia a la glucosa concluyeron que en los extractos acuosos en caliente de: Phyllantys niruri L. (Chancapiedra), Geranium dielsianum Knut (Pasuchaca), Gentianella alborosea G. (Hercampure), Otholobium pubescens (Culen) Smallantus sonchifolia (Yacón), Chloraphora tintoria (Mora) y Taraxacum officinalis W (Diente de león), se logró determinar vía analítica cualitativa la presencia del cromo, con el reactivo difenilcarbazida manifestándose a través de una coloración violeta o rojo. El análisis cuantitativo se determinó por Espectrofotometría de Absorción Atómica con los siguientes resultados en ppm: Gentianella alborosea G. (Hercampure) 0.030, Geranium dielsianum Knut ((Pasuchaca) 0.010, Phyllantus niruri L. (Chancapiedra) 0.050, Chloraphora tinctoria (Mora) 0.027, Taraxacum officinalis W. (Diente de León) 0.039, Otholobium pubescens (Culen) 3.2321, Smallantus sonchifolia (Yacón) 0.041.(3) tracto acuoso de Taraxacum officinalis Weber “diente de león” por vía oral en ratones albinos de la cepa CF1. • Existe una dosis mínima efectiva (DME) de 350 mg/Kg del extracto acuoso de Taraxacum officinalis Weber “diente de león” por presentar cromo en su composición para el efecto hipoglucemiante por vía oral ratones albinos de la cepa CF1.

JAMELÃO CONTRA A DIABETES

Fuente / Source

Repositório Institucional UNESP Produção científica Faculdade de Medicina (FMB) – Botucatu

Resumo
Diabetes mellitus (DM) é uma síndrome de etiologia múltipla caracterizada por hiperglicemia crônica. Esta hiperglicemia induz o aumento na produção de espécies reativas de oxigênio (ERO) e diminuição das defesas antioxidantes. Devido às complicações causadas pelo diabete, muitos indivíduos optam por terapias alternativas à base de plantas medicinais para amenizar seus efeitos. Sendo assim, nesta revisão de literatura, foram analisados e descritos diversos trabalhos experimentais com a utilização de animais diabéticos para comprovar os efeitos antioxidantes de algumas dessas plantas e verificar se os títulos e resumos disponibilizados nos artigos são compatíveis aos objetivos de nossa busca

Diabetes mellitus (DM) is a syndrome of multiple etiologies characterized by chronic hyperglycemia. This hyperglycemia induces increased production of reactive oxygen species (ROS) and decreased antioxidant defenses. Due to complications caused by diabetes, many people choose for alternative therapies and herbal medicine to alleviate its effects. Thus, in this literature review, several experimental studies with the use of diabetic animals were analyzed to demonstrate the antioxidant effects of some plants

Some plant species which have possible effects regarding diabetes mellitus (type 2):

Syzygium jambolanum

Descrição : Da família das Myrtaceae. Também conhecida como jamelão, azeitona, jalão, jambeiro, jambuí, oliva, oliveira.

Trata-se de uma árvore de porte alto, cultivada no Brasil. Os galhos e as folhas são colocados aos pares e os frutos são de coloração arroxeada, seus ramos e flores são dispostos em pares.

Seus frutos insípidos. Frutifica em fevereiro.

Parte utilizada: Cascas da árvore, folhas, sementes pulverizadas.

Habitat: E natural da Malásia, sendo encontrado na China, Austrália, Antilhas e Brasil, sendo comum em todo o país.

História: É usado pela população indígena e cabocla do país há centenas de anos. O fruto é consumido in natura e presta-se à fabricação de geléias.

Faz parte das farmacopéias ayurvédica e homeopática.

Princípios ativos:

Sementes: Ácidos graxos: ácidos – oléico, mlrístlco, palmítico, Iinoleico, esterculíaco, malvalico, vernólico taninos: corilagina,galoil-glucose, ácido 3,3′-di-0metil-elágico;

Cascas: taninos: ácidos derivados dos ácidos gálico e elágico; EsterÓides: B-sitosterol, glicosídeo do B-sitosterol;

Óleos essenciais: triterpenos – ácido betulínico, friedelina, eugenina, friedelanol. friedelana: Flavonóides: miricetina. kaempferol, quercetina, astragalina.

Princípios Ativos: Ácido ascórbico, ácido gálico, antimelina, betacaroteno, carboidratos, cariofileno, eugenol, homuleno, jambosina, limoneno, niacina, proteína, riboflavina, sais minerais (cálcio, cobre, enxofre, ferro, fósforo, magnésio, potássio sódio), tiamina, tanino.

Propriedades medicinais: Adstrigente, calmante, diurético, estomacal, hipoglicêmica, laxante, sudorífico.

Indicações: Diabetes, prisão de ventre, distúrbios gástricos e pancreáticos, disfunções nervosas, diabete, diarréia, espasmo, estimulante gastrointestinal, gases.

Uso pediátrico: As mesmas indicações posslvels.

Uso na gestação e na amamentação: Não há informações da sua farmacocinética ou sobre seu uso nestas condições.

Contra-indicações/cuidados: Paciêntes diabéticos em uso de qualquer planta, como tratamento complementar, devem ter sua glicemia constantemente monitorada e serem acompanhados por profissional gabaritado e ter acompanhamento clínico.

Jamelão

Posologia:

Adultos 9g de partes secas ou 2g de partes verdes (1 colher de sobremesa para cada xícara de água) de cascas ou sementes em decocto até 3 vezes ao dia, com intervalos menores que 12hs em

Uso interno (como chá ou gargarejos) ou Uso externo tópico em compressas e lavagens; Pó das sementes: 1 a 2g do pó dissolvido em água 3 vezes ao dia ou em dose única (30 sementes equivalem a 1,9g).

Precauções: Pacientes diabéticos em uso de qualquer planta, como tratamento complementar, devem ter sua glicemia constantemente monitorada e serem acompanhados por profissional gabaritado e ter acompanhamento clínico

Farmacologia: A atividade antiinflamatória foi demonstrada em experimentos com animais. A atividade hipoglicêmica ainda não foi comprovada. A casca tem atividade adstringente devido a seu alto teor de taninos.

Read more: plantasquecuram

Common treatment versus biological cure of the diabetic diseases and their later consequences

The common  symptomatic substitution treatment of Diabetes is based on the (wrong) presumption, that Diabetes would be incurable. Therefore, the treatment is limited to whipping on the B-cells to produce Insulin by a growing dosage of Sulfonyl urea, until the B-cells become exhausted. After that, the Insulin substitution follows, also needing from time to time an elevation of the dosages, until at last the matter gets out of control. In cases of Diabetes type I, immediately Insulin is injected. At the same time, carbohydrates are reduced in the nutrition, because the diabetic patient has only a reduced ability to process them.This biological method, however, aims at a cure of the disease by removing the true causes of the insufficient Insulin efficacy, and by re-establishing the natural basics of health, mainly by a man-appropriate natural nutrition. This normalizes the metabolic processes, and re-enables the patient to metabolize carbohydrates without the former limitations.  .luz vzl

moringa

Moringa Oleifera

Researchers recently reported that vitamin D is essential for the pancreas to be able to secrete insulin properly. The studies have shown that individuals with the lowest vitamin D levels experienced the worst blood sugar-handling problems and had a greater risk of developing diabetes. Moringa as a rich source of ascorbic acid helps in insulin secretion. It is interesting to note that certain nutrients like vitamins B1, B2, B12, pantothenic acid, vitamin C, protein and potassium – along with small frequent meals containing some carbohydrate – can actually stimulate production of insulin within the body.

Amino acids, lipid metabolites, and ferritin as potential mediators linking red meat consumption to type 2 diabetes

American Journal of Clinical Nutrition, 05/07/2015

Wittenbecher C, et al. – This study aimed to identify blood metabolites that possibly relate red meat consumption to the occurrence of type 2 diabetes. In the study, high ferritin, low glycine, and altered hepatic–derived lipid concentrations in the circulation were associated with total red meat consumption and, independent of red meat, with diabetes risk. The red meat–associated diabetes risk was largely attenuated after adjustment for selected biomarkers, which is consistent with the presumed mediation hypothesis.

Methods

  • Analyses were conducted in the prospective European Prospective Investigation into Cancer and Nutrition–Potsdam cohort (n = 27,548), applying a nested case-cohort design (n = 2681, including 688 incident diabetes cases).
  • Habitual diet was assessed with validated semiquantitative food-frequency questionnaires.
  • Total red meat consumption was defined as energy-standardized summed intake of unprocessed and processed red meats.
  • Concentrations of 14 amino acids, 17 acylcarnitines, 81 glycerophospholipids, 14 sphingomyelins, and ferritin were determined in serum samples from baseline.
  • These biomarkers were considered potential mediators of the relation between total red meat consumption and diabetes risk in Cox models.
  • The proportion of diabetes risk explainable by biomarker adjustment was estimated in a bootstrapping procedure with 1000 replicates.

Results

  • After adjustment for age, sex, lifestyle, diet, and body mass index, total red meat consumption was directly related to diabetes risk [HR for 2 SD (11 g/MJ): 1.26; 95% CI: 1.01, 1.57].
  • Six biomarkers (ferritin, glycine, diacyl phosphatidylcholines 36:4 and 38:4, lysophosphatidylcholine 17:0, and hydroxy-sphingomyelin 14:1) were associated with red meat consumption and diabetes risk.
  • The red meat–associated diabetes risk was significantly (P < 0.001) attenuated after simultaneous adjustment for these biomarkers [biomarker-adjusted HR for 2 SD (11 g/MJ): 1.09; 95% CI: 0.86, 1.38].
  • The proportion of diabetes risk explainable by respective biomarkers was 69% (IQR: 49%, 106%).

Adiponectina /

TECIDO ADIPOSO

 

Son los famosos "grasas indeseables ", ubicado debajo de la piel . El tejido adiposo es un tipo de tejido conectivo , su origen proviene de lipoblastos . Este tejido desempeña un papel importante en el cuerpo, tales como:

São as famosas “gordurinhas indesejáveis” localizadas em baixo da pele. O tecido adiposo é um tipo de tecido conjuntivo, sua origem advém dos lipoblastos. Este tecido desempenha um papel importante no nosso corpo como:

*isolante térmico;

*reserva de energia (os triglicerídeos); 

*proteção contra choques mecânicos;

Se han encontrado niveles bajos de adiponectina en pacientes diabeticos y hiper tensos. Los niveles plasmaticos son menores en hombres que en mujeres.androide.belly

En un estudio cientifico realizada se ha reportado que los bajos niveles de apiponectina se encuentran associados al grado de resistencia a la insulina . Hotta ha publicado una correlacion positiva entre adiponectina y colesterol de HDL en subjectos diabeticos tipo 2. Matsubara demostro que las concentraciones de adiponectina , se correlacionaban negativamente con los triglicéricos, el indice aterogénico (colesterol total /colesterol HDL).

adiponectina1Algunos autores han propuesto a la adiponectinacomo un confiable marcador de resistencia insulinica en la diabetes tipo 2. Yamauchi mostro que ratas tratadas con dosis fisiologicas de adiponectina disminuian significativamente (aunque no completamente), la hiperglicemia y hiperinsulinemia. Estudios experimentales han demonstrado que la adiponectina tiene propriedades antiaterogénicas y anit inflamatorias. La adhesion de los monocitos al endotilio vascular y la subsiguiente diferenciacion a macrofagos y cellulas espumosas es considerada crucial para el desarollo de la enfermedad vascular.

El gen de la adiponectina se encuentra ubicado en el cromosoma 3q27, jprecisamente donde se ha identificado el locus susceptible para la diabetes tipo 2 , el sindrome metabolico y la enfermedad coronaria. .

Kondo identifico 4 mutaciones de codigo erróneo en el dominio globular de la adiponectina . Por otro parte , el aumento en las concentraciones de adiponectina se accocia a un reducido riesgo de desarrolar diabetes tipo 2.

———————————————

Dislipidemia (Manejo del Paciente)

———————————————

En lo que refiere al balance calorico, la relacion de los aportes , segun el II Consejo Nacional (Venezolano) para pacientes con dislipidemias:

Alimentos                                                        Porcentage / o Gramos

Grasas poliinsaturadas                                     5%

Grasas monoinsaturadas                                 15%

Grasas saturadas                                               10 %

Carbohydratos                                                    45%

Proteinas                                                              15%

Fibras solubles                                                    30 gr

Plantas (Fitoquimicos) ricas en estanoles y esteroles    2 gr

Colesterol                                                             300 gr

Se recomienda el incremento de fibra soluble (goma, pectinas, hemicelulosas contendidas en avenas , cebada, legumbres, ciruela, lechosa, manzana, zanahoria, y naranja. y fibra insoluble como trigo, maiz, granos oleaginosos, frutas y hortalizas.

Fitoquimicos

Estan constituidos por plantas cuya propriedad principal es su accion antioxidante: Esteroles, flavonoides fenólicos y licopenos.

Los esteroles , aunque paracidos al colesterol animal se diferencian de este por su origen vegetal y son los siguienes : sitosterol, estigmasterol, y campesterol.. El aceite de canola (linaza) oriundo de Canada, contiene ésteres de sitostanol, que en consumo de 3-a 4 gramos diarios disminuye el LDL, hasta un 10 % sin effecto sobre HDL ni triacilglicéridos , lo cual se atribuye a interupción del transporte transmembrana intestinal por alteración de la esterificación del colesterol (www. canolainfo.org).

Los flavonoides fenólicos tienen propriedad antioxidante y se encuentran en semillas oleaginosas (mani, merey, amendra, nueces, piñones, ajonjoli, ) mientras que los flavonoles y flacones antocianinas estan contenidos en la cebolla. soya e vino. Los fenoles se encuentran en el vino tintoy disminuyen la oxidacion de la LDL.

Otra sustancia antioxidante es el licopeno , pigmento soluble de color rojo contenido en la patilla, guayaba, tomate, toronja rosada y que junto con los carotenos constituye los carotenoides, los cuales contribuyen a controlar el engrosamiento de la intima carotidea (Am J. Clin Nutr 2003 ..33-138)almonds Los fosfatos aportado por las frutas , verduras y vegetales proprio del tropico, Brasil. Colombia, Venezuela -aportan los 180mcg de ácido folico, recomendado disminuir el riesgo cardiovascular.

cebolla

Diabetes y obesidad: su relación con el exceso
de grasas en la  alimentación
—————————————————————————-
Un estudio de la Universidad de Michigan (EE UU) lo confirma

Las comidas con altos contenidos de grasa pueden contribuir a la obesidad, lo cual incrementa el riesgo de desarrollar la diabetes tipo 2. Un estudio de laboratorio del Sistema de Salud de la Universidad de Michigan [1] proporciona nuevas claves acerca de los cambios moleculares perjudiciales para la salud que se inician al comer alimentos con altos contenidos de grasa y apunta a una proteína que inicia el efecto dañino de la glotonería: un mejor entendimiento de la respuesta del cuerpo a la glotonería podría conducir a nuevos enfoques en el tratamiento de la diabetes y el síndrome metabólico.

Diabetes y obesidad: su relación con el exceso de grasas en la alimentación(imagen La hiperglicemia suele cursar con decaimiento, fatiga, malestar general, náuseas y vómitos, así como dificultad para respirar wikipedia).

Los investigadores encontraron que una proteína clave, llamada Bcl10 es necesaria para que los ácidos grasos libres, que se encuentran en las comidas con elevado contenido de grasa y se almacenan en la grasa del cuerpo, obstruyan la acción de la insulina y lleven a niveles anormalmente elevados de azúcar en la sangre.

En el estudio hecho en el laboratorio a ratones con deficiencia de la proteína Bcl10 se les protegió del desarrollo de resistencia a la insulina mediante la alimentación con una dieta de alto contenido graso. Las conclusiones se publicarán el 31 de mayo en la revista Cell Reports.

La insulina ayuda a controlar el azúcar en la sangre, pero la resistencia a la insulina puede conducir a niveles anormalmente altos de azúcar en la sangre que son la característica de la diabetes. La resistencia a la insulina puede ocurrir como parte del síndrome metabólico, un conjunto de condiciones que incrementa el riesgo de desarrollar la diabetes tipo 2 y enfermedades cardiacas.

En la actualidad millones de personas en Estados Unidos tienen exceso de peso o son obesas, a la vez que aumentan la diabetes tipo 2 y el síndrome metabólico.

El estudio muestra asimismo cómo los cambios de muy corto plazo en la dieta, como por ejemplo el comer comidas con alto contenido graso por unos pocos días, y aún menos quizá, puede inducir un estado de resistencia a la insulina”, dijo el autor senior del estudio Meter C. Lucas, profesor asociado de patología en la Escuela de Medicina de la Universidad de Michigan.

Los investigadores comenzaron estudiando la forma en que los ácidos grasos libres inducen la inflamación y obstruyen la acción de la insulina en el hígado. Se cree que el hígado es un blanco principal para los efectos dañinos de los ácidos grasos libres.

En el hígado los ácidos grasos libres son metabolizados y producen diacilgliceroles antes de inducir la respuesta inflamatoria. Los diacilgliceroles también activan el señalador NF-kB que se ha vinculado con el cáncer y las enfermedades metabólicas y vasculares.

El equipo investigador concluyó que se necesita de la Bcl10 para que los ácidos grasos induzcan la inflamación y la resistencia a la insulina. En el estudio los ratones con deficiencia de Bcl10 mostraron una mejoría significativa en la regulación del azúcar en la sangre.

Nos sorprendió encontrar que la Bcl10, una proteína que antes se conocía por su papel crítico en la respuesta celular de inmunidad a la infección, desempeña también un papel crítico en la respuesta del hígado a los ácidos grasos”, dijo Lucas: “Éste es un ejemplo de cómo la naturaleza se apropia de un mecanismo fundamental para el sistema de inmunidad y lo usa en un órgano metabólico, en este caso el hígado”.

Estas conclusiones”, dijo la coautora senior Lynda McAllister Davis, profesora asociada de hematología y oncología pediátricas, “revelan un papel nuevo e importante para la Bcl10, y podrían conducir a ideas novedosas en el tratamiento de los pacientes con síndrome metabólico y diabetes tipo 2”.

Autores adicionales: Matthew Van Beek, Katherine I. Oravecz-Wilson, Phillip C. Delekta, Shufang Gu, Xiangquan Li, Xiaohong Jin, Ingrid J. Apel, Katy S. Konkle, Yongja Feng y Daniel H. Teitelbaum de la UM; y Jurgen Ruland, del Institut fur Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, Technische Universitat Munchen, Munich, Alemania, y el Laboratorio de Señalización del Sistema de Inmunidad, Helmholtz Zentrum Munchen-Alemania, Centro de Investigación para la Salud Ambiental, Nuremberg, Alemania.

Argenpress

(23 de mayo de 2012)

Diabetes Tipo 2

Não use medicamento sem o conhecimento do seu
médico. Pode ser perigoso para a sua

saú

Diabetes y obesidad: su relación con el exceso de grasas en la alimentación
Un estudio de la Universidad de Michigan (EE UU) lo confirma

Las comidas con altos contenidos de grasa pueden contribuir a la obesidad, lo cual incrementa el riesgo de desarrollar la diabetes tipo 2. Un estudio de laboratorio del Sistema de Salud de la Universidad de Michigan [1] proporciona nuevas claves acerca de los cambios moleculares perjudiciales para la salud que se inician al comer alimentos con altos contenidos de grasa y apunta a una proteína que inicia el efecto dañino de la glotonería: un mejor entendimiento de la respuesta del cuerpo a la glotonería podría conducir a nuevos enfoques en el tratamiento de la diabetes y el síndrome metabólico.

Diabetes y obesidad: su relación con el exceso de grasas en la alimentación(imagen La hiperglicemia suele cursar con decaimiento, fatiga, malestar general, náuseas y vómitos, así como dificultad para respirar wikipedia).

Los investigadores encontraron que una proteína clave, llamada Bcl10 es necesaria para que los ácidos grasos libres, que se encuentran en las comidas con elevado contenido de grasa y se almacenan en la grasa del cuerpo, obstruyan la acción de la insulina y lleven a niveles anormalmente elevados de azúcar en la sangre.

En el estudio hecho en el laboratorio a ratones con deficiencia de la proteína Bcl10 se les protegió del desarrollo de resistencia a la insulina mediante la alimentación con una dieta de alto contenido graso. Las conclusiones se publicarán el 31 de mayo en la revista Cell Reports.

La insulina ayuda a controlar el azúcar en la sangre, pero la resistencia a la insulina puede conducir a niveles anormalmente altos de azúcar en la sangre que son la característica de la diabetes. La resistencia a la insulina puede ocurrir como parte del síndrome metabólico, un conjunto de condiciones que incrementa el riesgo de desarrollar la diabetes tipo 2 y enfermedades cardiacas.

En la actualidad millones de personas en Estados Unidos tienen exceso de peso o son obesas, a la vez que aumentan la diabetes tipo 2 y el síndrome metabólico.

El estudio muestra asimismo cómo los cambios de muy corto plazo en la dieta, como por ejemplo el comer comidas con alto contenido graso por unos pocos días, y aún menos quizá, puede inducir un estado de resistencia a la insulina”, dijo el autor senior del estudio Meter C. Lucas, profesor asociado de patología en la Escuela de Medicina de la Universidad de Michigan.

Los investigadores comenzaron estudiando la forma en que los ácidos grasos libres inducen la inflamación y obstruyen la acción de la insulina en el hígado. Se cree que el hígado es un blanco principal para los efectos dañinos de los ácidos grasos libres.

En el hígado los ácidos grasos libres son metabolizados y producen diacilgliceroles antes de inducir la respuesta inflamatoria. Los diacilgliceroles también activan el señalador NF-kB que se ha vinculado con el cáncer y las enfermedades metabólicas y vasculares.

El equipo investigador concluyó que se necesita de la Bcl10 para que los ácidos grasos induzcan la inflamación y la resistencia a la insulina. En el estudio los ratones con deficiencia de Bcl10 mostraron una mejoría significativa en la regulación del azúcar en la sangre.

Nos sorprendió encontrar que la Bcl10, una proteína que antes se conocía por su papel crítico en la respuesta celular de inmunidad a la infección, desempeña también un papel crítico en la respuesta del hígado a los ácidos grasos”, dijo Lucas: “Éste es un ejemplo de cómo la naturaleza se apropia de un mecanismo fundamental para el sistema de inmunidad y lo usa en un órgano metabólico, en este caso el hígado”.

Estas conclusiones”, dijo la coautora senior Lynda McAllister Davis, profesora asociada de hematología y oncología pediátricas, “revelan un papel nuevo e importante para la Bcl10, y podrían conducir a ideas novedosas en el tratamiento de los pacientes con síndrome metabólico y diabetes tipo 2”.

Autores adicionales: Matthew Van Beek, Katherine I. Oravecz-Wilson, Phillip C. Delekta, Shufang Gu, Xiangquan Li, Xiaohong Jin, Ingrid J. Apel, Katy S. Konkle, Yongja Feng y Daniel H. Teitelbaum de la UM; y Jurgen Ruland, del Institut fur Klinische Chemie und Pathobiochemie, Klinikum rechts der Isar, Technische Universitat Munchen, Munich, Alemania, y el Laboratorio de Señalización del Sistema de Inmunidad, Helmholtz Zentrum Munchen-Alemania, Centro de Investigación para la Salud Ambiental, Nuremberg, Alemania.

Argenpress

(23 de mayo de 2012)

de.

Please do not use this medicine without prior knowledge of your physician. It may be dangerous to your health.

Byetta is injected twice daily, and Victoza is injected once a day. Bydureon, a newer formulation, is injected once a week. These drugs do have different effects and side effects to consider.

  • Exenatide (Byetta, Bydureon). The most common side effect of exenatide is mild to moderate nausea, which improves with time in most people. Several cases of kidney problems, including kidney failure, have been reported in people who have taken exenatide. Rarely, exenatide may cause harmful inflammation of the pancreas (pancreatitis).
1 CDS 03AGO11
BYETTA ®
exenatida
D.C.B. 09381
APRESENTAÇÕES
BYETTA é uma solução injetável isotônica, preservada e estéril
BYETTA®
exenatida
APRESENTAÇÕES
BYETTA é uma solução injetável isotônica, preservada e estéril
,
contendo 250 mcg de
exenatida sintética por
m
L
. BYETTA é apresentado nas seguintes embalagens:
Embalagem contendo 1 caneta injetora com cartucho
COMPOSIÇÃO
Cada mL contém: exenatida ………………
250 mcg
Excipientes: metacresol, manitol, ácido acético glacial, acetato trihidratado de sódio e água para
injeção.
INFORMAÇÕES AO
PACIENTE
PARA QUE
ESTE MEDICAMENTO É INDICADO?
BYETTA é indicado como tratamento auxiliar para a melhora do controle da taxa de glicose no
sangue em pacientes com
diabetes mellitus
tipo 2 e que estejam tomando metformina,
sulfonilureia (medicamentos que reduz em a quantidade
de glicose no sangue) ou uma combinação de metformina e sulfonilureia, mas que não tenham atingido um controle adequado
de glicose no sangue.
BYETTA é indicado como tratamento auxiliar para a melhora do controle da taxa de glicose no sangue em pacientes com
diabetes mellitus tipo 2 e IMC > 25kg/m2 e que estejam tomando uma tiazolidinediona (medicamento que ajuda a reduzir a quantidade de glicose no sangue), ou uma combinação de tiazolidinediona e metformina, mas que não tenham atingido um controle
adequado de glicose no sangue.
BYETTA é indicado para a melhora do controle da taxa de glicose no sangue em pacientes com diabetes mellitus tipo 2 e IMC > 25 kg/m
2 em combinação com uma insulina basal /longa duração
com ou sem metformina e/ou tiazolidinediona
.
COMO ESTE MEDICAMENTO FUNCIONA?
BYETTA melhora o controle da taxa de glicose (açúcar) no sangue em pacientes com diabetes mellitus tipo 2
, aumentando a secreção de insulina pelo pâncreas (uma glândula situada perto do estômago), reduzindo
a secreção inadequadamente alta de glucagon (hormônio responsável por aumentar a taxa de glicose no sangue) e lentificando o esvaziamento do estômago.
O tempo médio esperado para o início da ação farmacológica de BYETTA é dentro de 30 minutos após injeção subcutânea.
QUANDO NÃO DEVO USAR ESTE MEDICAMENTO?
Não use BYETTA caso seja alérgico a exenatida e/ou a qualquer um dos componentes da fórmula
SOMENTE PARA ADMINISTRAÇÃO SUBCUTÂNEA
BRAND NAME: Byetta, Bydureon

DRUG CLASS AND MECHANISM: Exenatide is an injectable drug that reduces the level of sugar (glucose) in the blood. It is used for treating type 2 diabetes. Exenatide belongs in a class of drugs called incretin mimetics because these drugs mimic the effects of incretins. Incretins, such as human-glucagon-like peptide-1 (GLP-1), are hormones that are produced and released into the blood by the intestine in response to food. GLP-1 increases the secretion of insulin from the pancreas, slows absorption of glucose from the gut, and reduces the action of glucagon.

(Glucagon is a hormone that increases glucose production by the liver.) All three of these actions reduce levels of glucose in the blood. In addition, GLP-1 reduces appetite.

Exenatide is a synthetic (man-made) hormone that resembles and acts like GLP-1. In studies, exenatide-treated patients achieved lower blood glucose levels and experienced weight loss. Exenatide was approved by the FDA in May 2005.]]

Romero y orégano contra la diabetes 2

Jueves, 24 julio 2014
Por Editor elclarin
Romero y orégano contra la diabetes 2

Fuente Univisión.com/Foto: Univisión.com |Los hallazgos publicados en la revista Journal of Agricultural and Food Chemistry de la Asociación Química Estadounidense (ACS, por sus siglas en inglés), refieren que ambas hierbas aromáticas son fuentes concentradas de polifenoles y flavonoides que inhiben a la enzima Dipeptidil Peptidasa IV (DPP-4) y a la proteína tirosina fosfatasa 1B (PTP1B), que juegan un rol clave en la secreción de insulina y la señalización de la insulina, respectivamente.

Para llegar a dicha conclusión, los investigadores evaluaron la capacidad de cuatro hierbas diferentes, de interferir con la DPP-4 y la PTP1B, el orégano griego (Origanum vulgare), la mejorana (Origanum majorana), el romero (Rosmarinus officinalis) y orégano mexicano (Lippia graveolens), en sus versiones comerciales secas y cultivadas en invernadero.

Si bien, descubrieron que las hierbas cultivadas en invernadero contienen más polifenoles y flavonoides en comparación con las versiones comerciales, esto no afectó la concentración requerida para bloquear la enzima. El orégano griego, orégano mexicano y romero fueron los mejores inhibidores.

Aunque los resultados son prometedores, los autores del estudio reconocieron que se requieren más estudios para entender el papel de estos compuestos en la reducción de nivel de glucosa en sangre en las personas que viven con diabetes tipo 2.

Otras propiedades del romero

Natural Standard, empresa de investigación internacional sobre medicina alternativa, destaca que los componentes del romero más investigados son el ácido cafeico y su derivado, el ácido rosmarínico. Se cree que estos componentes tienen efectos antioxidantes y se estudian actualmente como terapias potenciales para cáncer, hepatotoxicidad (toxicidad del hígado) y afecciones respiratorias.

Actualmente, los estudios disponibles muestran al romero como promisorio en el tratamiento de la ansiedad/el estrés (aromaterapia) y alopecia (pérdida de cabello). Los usos cosméticos actuales del romero incluyen el tratamiento de celulitis y arrugas, y la normalización de la secreción excesiva de aceite de la piel. La Comisión E de Alemania aprobó el uso del romero para el tratamiento de la dispepsia, y el aceite de romero (uso externo) para el dolor de articulaciones y escasa circulación.

……………………………………………………………………………………………………………..

Dr. Cristofore NIKO Link, Dieta & Manejo Nutríco –Medicina Botânica
Post-Graduación M.I.T – Ex Prof.Medicina LUZ MIT UNLV RU

Pierde 4kg cada mes sin fármacos . Dr C. NIKO http://www.doutorniko.wordpress.com

Email: nikolink(at) live.com
• Dr Cristoforé NIKO Obesidad – Diabetes & Terapias Botánicas

”””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””””” norwegian-flag

Fast food increases postprandial cardiac workload in type 2 diabetes independent of pre-exercise:

…………………………………………………………………………………………………………………………………………………..
Siri Marte Hollekim-Strand1, Vegard Malmo12, Turid Follestad3, Ulrik Wisløff1 and Charlotte Björk Ingul1* * Corresponding author: Charlotte B Ingul charlotte.b.ingul@ntnu.no Author Affiliations
1 K.G. Jebsen Centre of Exercise in Medicine at Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, 7491, Norway 2 Department of Cardiology, St. Olavs Hospital, Trondheim, Norway 3 Department of Public Health and General Practice, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway Nutrition Journal 2015, 14:79 doi:10.1186/s12937-015-0069-1
Abstract Background
Type 2 diabetes aggravates the postprandial metabolic effects of food, which increase cardiovascular risk. We investigated the acute effects of fast food on postprandial left ventricular (LV) function and the potential effects of pre-exercise in type 2 diabetes individuals.
Methods We used a cross-over study including 10 type 2 diabetes individuals (7 male and 3 females; 53.4 ± 8.1 years; 28.3 ± 3.8 kg/m 2 ; type 2 diabetes duration 3.1 ± 1.8 years) and 10 controls (7 male and 3 females; 52.8 ± 10.1 years; 28.5 ± 4.2 kg/m 2 ) performing high intensity interval exercise (HIIE; 40 min, 4 × 4min intervals, 90–95 % HR max ), moderate intensity exercise (MIE; 47 min, 70 % HR max ) and no exercise (NE) in a random order 16–18 hours prior to fast-food ingestion. Baseline echocardiography, blood pressure and biochemical measurements were recorded prior to and 16–18 hours after exercise, and 30 minutes, 2 hours and 4 hours after fast food ingestion. Results LV diastolic (peak early diastolic tissue velocity, peak early diastolic filling velocity), and systolic workload (global strain rate, peak systolic tissue velocity, rate pressure product) increased after consumption of fast food in both groups. In contrast to controls, the type 2 diabetes group had prolonged elevations in resting heart rate and indications of prolonged elevations in diastolic workload (peak early diastolic tissue velocity) as well as reduced systolic blood pressure after fast food consumption. No significant modifications due to exercise in the postprandial phase were seen in any group.
Conclusions
Our findings indicate that fast-food induces greater and sustained overall cardiac workload in type 2 diabetes individuals versus body mass index and age matched controls; exercise 16–18 hours pre-meal has no acute effects to the postprandial phase.
Trial registration
ClinicalTrials.gov: NCT01991769.
Background
Most of the day is spent in the postprandial state and frequent ingestion of energy dense food, rich in processed carbohydrates, saturated fats and salt (fast-food), increases the risk of cardiometabolic diseases [1]–[3].
Type 2 diabetes aggravates the postprandial metabolic effects of food because it impairs the transport, delivery and/or storage of carbohydrates and fats [4]. Although type 2 diabetes is an accepted cause of heart failure [5] and approximately 50 % of asymptomatic individuals with well-controlled type 2 diabetes show signs of diastolic dysfunction [6], little is known about the acute effects of food in the view of cardiac function in this population.
Endothelial function is impaired after fast food ingestion, which is related to increases in circulating glucose, triglycerides and/or elevated oxidative stress [7], [8]. However little is known about the acute consequence of excessive elevations in circulating glucose and/or triglycerides after a meal on cardiac function in type 2 diabetes.
Although few studies have investigated the acute effects of fast food on cardiac function, it is observed that food-induced elevation of circulating glucose and oxidative stress reduce diastolic function in insulin-treated type 2 diabetes patients [9], and that acute elevations in circulating triglycerides yield compensatory increases in systolic function of the left ventricle in healthy individuals [10].
Chronic exercise improves cardiac function [6] and even single bouts of exercise can improve endothelial function, triglycerides and oxidative stress in healthy and reduce postprandial glucose elevations in type 2 diabetes individuals [8], [11], [12]. Exercise 16–18 hours pre-meal has previously shown to induce improvements in total antioxidant status (TAS) and endothelial function, rather than reduce the circulating glucose or triglycerides [8]. In this setting, high intensity interval exercise (HIIE) was more effective in improving postprandial endothelial function compared to moderate intensity exercise (MIE) [8].
No study has investigated whether fast food ingestion induces an acute increase in cardiac workload, or whether this may be modified by pre-exercise as observed for endothelial function [8].
The purpose of this study was thus to explore whether a single fast food meal affects left ventricular (LV) diastolic and systolic function in the four hour postprandial phase, and whether exercise (HIIE or MIE) 16–18 hours prior to a single fast food meal could affect LV function, resting heart rate, blood pressure and/or other biochemical measures in type 2 diabetes patients.
Methods
Study participants
Type 2 diabetes individuals and healthy controls were recruited through a local newspaper and from advertisement at St. Olav’s University hospital, Trondheim, Norway. The study was performed from February to June 2012.
The inclusion criteria included: age 40 to 65 years and type 2 diabetes within the past 10 years with no use of insulin. Exclusion criteria included: known cardiovascular or lung disease, uncontrolled hypertension, orthopaedic or neurological restrictions, body mass index (BMI) >35 kg/m 2 , pregnancy, inability to exercise, smoking, drug or alcohol abuse, planned surgery during the trial period, serious eating- and/or personality disorders, reluctance to sign informed consent form, or more physical activity than today’s recommendations [13].
Ten type 2 diabetes individuals and 10 healthy age and BMI matched controls were included. The protocol was approved by the Regional Committee for Medical and Health Research Ethics and registered in the Clinical Trials Registry (ClinicalTrials.gov identifier: NCT01991769). Informed consent was obtained from all participants.
Design
A minimum of one week before the first trial, peak oxygen uptake (VO 2peak ) was assessed (Jaeger LE2000CE, Hochberg, Germany) as previously described [14]. Each of the 20 subjects participated in all trials (HIIE, MIE and no exercise (NE)), in a randomized order with a minimum of one week between trials. The timeline representing each trial is illustrated in Figs. 1, 2, 3 and 4. Baseline-1 measurements were performed on the day prior to fast-food ingestion in a resting (sedate behavior/refrained from exercise, ≥48 hours) and fasting (≥12 hours) state that abstained from caffeine, citrus and alcohol (16–18 hours). During the 16–18 hour period after HIIE, MIE or NE, the subjects were instructed to abstain from exercise, caffeine, citrus and alcohol and to report for baseline-2 in a fasting (≥12 hours) state the following morning. Before overnight fasting commenced, prior to all baseline-1 and baseline-2 measurements, subjects ingested a mixed meal at the same time and of the same content (same manufacturer, same amount) as they did before baseline-1 in their first trial. This meal was typically a standard Norwegian supper (i.e., whole grain sandwich with butter/margarine and meat/egg/fish/cheese and milk or water). Following baseline-2, fast food was ingested and measurements performed 30 minutes, 2 hours and 4 hours after the meal. The participants remained inactive in the laboratory after fast-food ingestion until end of the protocols.
Fig. 1. Effects of fast food (left panel; all trials combined) and exercise (right panel; high intensity interval exercise +moderate intensity exercise vs. no exercise) on left ventricular diastolic function. Abbreviations: BL, baseline; C, control group; e’, peak early diastolic tissue Doppler velocity; E/e’ , filling pressure; E, peak early filling velocity; HIIE, high intensity interval exercise; HIIE+MIE, exercise combined; IVRT, isovolumic relaxation time; MIE, moderate intensity exercise; NE, no exercise; T2D, type 2 diabetes group. Estimated means and 95 % CIs from LMMs with the factors time, group and their interaction (left panel, figures a-d), and with the factors time, group, trial and their interactions (right panel, figures E-H). In the left panel significant (p < 0.01) time differences are indicated by *(from BL1), † (from BL2), ‡ (from food +30 min) and § (from food +2 h). For peak early filling velocity (e) there is no significant time and group interaction, and the indicated significant time differences refer to the main effect of time for both groups
Fig. 2. Effects of fast food (left panel; all trials combined) and exercise (right panel; high intensity interval exercise +moderate intensity exercise vs. no exercise) on left ventricular systolic function. Abbreviations: BL, baseline; C, control group; HIIE, high intensity exercise; HIIE+MIE, exercise combined; MIE, moderate intensity exercise; NE, no exercise; S’ , peak systolic tissue Doppler velocity; T2D, type 2 diabetes group. Estimated means and 95 % CIs from LMMs with the factors time, group and their interaction (left panel, figures a-b), and with the factors time, group, trial and their interactions (right panel, figures c-d). In the left panel significant (p < 0.01) time differences are indicated by *(from BL1), † (from BL2), ‡ (from food +30 min) and § (from food +2 h). For S’ and global strain rate there is no significant time and group interaction, and the indicated significant time differences refer to the main effect of time for both groups
Fig. 3. Effects of fast food (left panel; all trials combined) and exercise (right panel; high intensity interval exercise+moderate intensity exercise vs. no exercise) on resting heart rate and blood pressure. Abbreviations: BL, baseline; BP, blood pressure; C, control group; HIIE, high intensity exercise; HIIE+MIE, exercise combined; HR, resting heart rate; MIE; moderate intensity exercise; NE, no exercise; RPP, rate pressure product; T2D, type 2 diabetes group. Estimated means and 95 % CIs from LMMs with the factors time, group and their interaction (left panel, figures a-d), and with the factors time, group, trial and their interactions (right panel, figures e-h). In the left panel significant (p < 0.01) time differences are indicated by *(from BL1), † (from BL2), ‡ (from food +30 min) and § (from food +2 h). For diastolic BP there is no significant time and group interaction, and the indicated significant time differences refer to the main effect of time for both groups. For RPP, the means and CIs are shown as back-transformed values, computed by direct exponentiation of the means and CIs from the LMM based on log-transformed data
Fig. 4. Effects of fast food (left panel, trials combined) and exercise (right panel; high intensity interval exercise+moderate intensity exercise vs. no exercise) on blood glucose, C-peptide, triglycerides and total antioxidant status. Abbreviations: BL, baseline; C, control group; HIIE, high intensity exercise; HIIE+MIE, exercise combined; MIE, moderate intensity exercise; NE, no exercise; TAS, total antioxidant status; T2D, type 2 diabetes group. Estimated means and 95 % CIs from LMMs with the factors time, group and their interaction (left panel, figures a-d), and with the factors time, group, trial and their interactions (right panel, figures e-h). In the left panel significant (p < 0.01) time differences are indicated by *(from BL1), † (from BL2), ‡ (from food +30 min) and § (from food +2 h). For triglycerides there is no significant time and group interaction, and the indicated significant time differences refer to the main effect of time for both groups. Except for TAS, the means and CIs are shown as back-transformed values, computed by direct exponentiation of the means and CIs from the LMMs based on log-transformed data
Outcome measures
The primary outcome measure was LV diastolic function measured as peak early diastolic tissue velocity (e’). Secondary outcome measures were LV late diastolic tissue velocity (a’), LV early diastolic filling velocity (E), LV late diastolic filling velocity (A), LV filling pressure (E/e’), E/A-ratio, deceleration time (DT), isovolumic relaxation time (IVRT), LV global strain and strain rate, LV peak systolic tissue velocity (S’) as well as resting heart rate, blood pressure, circulating glucose, triglycerides, total cholesterol, LDL-cholesterol, HDL-cholesterol, C-peptide, total antioxidant status (TAS) and high sensitive c-reactive protein (hs-CRP).
Exercise training protocols
All exercise trials were supervised. HIIE was performed by walking or running on an inclined treadmill. Following 10 min warm up at approximately 70 % of maximal heart rate obtained at exercise testing (HR max ), the HIIE-group performed four intervals at 90-95 % of HR max with 3 minutes recovery periods between intervals at 70 % of HR max and 5 minutes cool down; 40 min altogether. The MIE protocol consisted of 47 minutes exercise at 70 % of HR max to achieve approximately similar total energy expenditure as for HIIE.
Fast food
The fast food consisted of a vegetarian mozzarella pizza (Dr. Oetker); 335 g (874 kcal/ 3655 kJ), 83.4 g carbohydrates, 44.2 g fat, and 34.8 g protein. A previous study indicated that this pizza induces a marked postprandial increase in circulating glucose, triglycerides, C-peptide and a decrease in TAS as well as a transient impairment in endothelial function in healthy individuals [8].
Clinical and laboratory examinations
Resting echocardiography
Three consecutive cycles in B-mode acquisitions (mean frame rate 53/sec) and color tissue Doppler imaging (TDI) (mean frame rate 159.9/sec) were recorded from the 3 apical views (four-chamber, two-chamber, and long- axis) and B-mode from the parasternal view. Measurements included E, A, IVRT and DT. Pulsed wave tissue Doppler velocities were measured at the four mitral annular sites in the four-chamber and two-chamber views. The mean of these points was used for S’ , e’ and a’ [15]. The ratio E/e’ was calculated as an estimate of LV filling pressure [16]. Global strain and strain rate were calculated from 2-dimensional strain echocardiography [17]. Measurements obtained in this study are in accordance with standard procedures recommended by the American Society of Echocardiography [18], and no subjects were excluded because of impaired echocardiographic image quality. Images were analyzed off line using EchoPAC version BT12 (GE Vingmed Ultrasound, Horten, Norway). The observer was blinded to group participation, trial and point in time during ultrasound analysis.
Resting heart rate and blood pressure
The lowest heart rate observed during echocardiography was defined as the resting heart rate. Upright blood pressure measurements were performed using Philips SureSigns V52 (Andover, Massachusetts, US). Before baseline-1 and baseline-2, participants rested in a sitting position for at least 10 minutes before measurements. Blood pressure at these time points was noted as the median of three recordings. At the remaining time points, upright blood pressure was measured only once. Rate pressure product (RPP; heart rate x systolic blood pressure) was calculated to determine myocardial workload.
Biochemical analysis
Blood was collected after blood pressure measurements and before echocardiography. Blood glucose, C-peptide, plasma triglycerides, total cholesterol, high density lipoprotein (HDL) and low density lipoprotein (LDL) and high-sensitive C-reactive protein (hs-CRP) were analyzed according to standard procedures at the St. Olavs Hospital (Trondheim) at all time-points; HbA 1c was measured at baseline-1. Blood glucose was measured using photometric hexokinase UV method (Roche Modular, Roche Diagnostics, Germany) and C-peptide was measured using chemiluminescence method (Immulite 2000, Siemens Medical Solutions, New Jersey, US). The blood lipids were measured using photometric, enzymatic colorimetric method (Roche Modular, Roche Diagnostics Germany). Hs-CRP was measured using Tina-quant CRPHS immunoturbidimetric assay (Roche Modular, Roche Diagnostics, Germany). HbA 1c was measured using TINIA (Turbidimetric Inhibition immunoassay) (Roche Cobas Integra 400 plus, Roche Diagnostics, Germany). Insulin sensitivity was calculated using the HOMA2 calculator (The Homeostasis Assessment Model, University of Oxford, UK). Total antioxidant status (TAS) was analyzed as previously described [19].
Statistical methods
The statistical analysis was performed by linear mixed models (LMMs). Within-subject correlations were considered using a random intercept in the LMM. A full model included group (type 2 diabetes or controls), trial (HIIE, MIE, or NE), and time (baseline-1, baseline-2, and 30 minutes, 2 hours and 4 hours post-meal). Models with two levels of the trial factor (HIIE and MIE combined or NE) were also considered. Tests for overall effects of factors and factor interactions were done by likelihood ratio tests using significance level 0.05. Post hoc comparisons specified and tested appropriate linear combinations (contrasts) of the estimated model parameters for the selected models. In all models, the baseline means (baseline-1) for each group were restricted to be equal for the three exercise trials due to randomization to trials within each group [20]. Outcome variables not meeting the normal assumptions of the LMM were log transformed prior to the statistical analysis in cases where this transformation improved the approximation to the normal distribution. The analyses were performed in the R statistical package [21].
This study is explorative rather than confirmative, and thus we did not perform any formal adjustment for multiple testing. However, if nothing else is explicitly stated, the results presented and discussed here are statistically significant at p<0.01.
Results
Subject characteristics
Subject characteristics are reported in Table 1. Twenty participants completed all trials (HIIE, MIE, NE), and exercised according to prescribed exercise heart rates and followed instructions of sedentary behavior during the NE trial. No adverse events were reported. Since no statistically significant effects of pre-exercise were found, the results discussed below are from LMMs including the factors group and time.
Table 1. Subject characteristics
Effect of pre-exercise
Since no statistically significant effects of pre-exercise were found, the results discussed below are from LMMs including the factors group and time.
Cardiac function
The LV diastolic responses to fast food are illustrated in Fig. 1a-d.
The type 2 diabetes group had an overall poorer diastolic function (e’) and higher filling pressure (E/e’) versus controls (Fig. 1a-b).
In general, diastolic workload increased (higher e’ , a’ , E and A) within 30 minutes after the meal in both groups. Subsequently, diastolic workload reversed towards baseline-2 levels, but in contrast to controls (p = 0.10), the type 2 diabetes group showed an indication of increased diastolic workload as measured by e’ that persisted 4 hours after the meal (p = 0.02). Late diastolic filling (a’) remained elevated 4 hours after fast food in both groups.
Filling pressure (E/e’) and isovolumic relaxation time (IVRT) were reduced within 2 hours after the meal in the type 2 diabetes group; this was not significantly different after fast food in the controls. The difference between groups in change from baseline-2 to 2 hours post-meal was almost significant for IVRT (p = 0.03) but not for filling pressure (p = 0.08). No effect of time was observed for E/A ratio because both E and A increased. Supernormal filling is associated with vigorous recoil of the ventricle during diastole with an increase of negative pressure in the ventricle and evacuation of blood from the atrium. This causes a high E wave, shortening of the IVRT and normal deceleration time. We found that the shortened IVRT and lack of changes to deceleration time might be due to the same mechanism.
Pre-exercise did not influence postprandial early diastolic velocity (e’) (Fig. 1e) or any other diastolic echocardiographic variables (Fig. 1f-h).
The LV systolic response to fast food are illustrated in Fig. 2a-b. In general, systolic workload (global strain rate and S’) increased 30 min after the meal in both groups. Systolic workload was subsequently reversed, but remained significantly elevated (global strain rate and S’) compared to baseline-2 after 4 hours in both groups (Fig. 2a-b).
Pre-exercise did not affect systolic function (Fig. 2c-d).
Hemodynamic measurements
The heart rate, blood pressure and RPP responses to fast food are illustrated in Fig. 3a-d.
The type 2 diabetes group had an increased heart rate versus controls (p < 0.01 or p < 0.05) at all time-points except 30 minutes after fast food (p = 0.06). Resting heart rate increased within 30 minutes after the meal and subsequently decreased in both groups; it decreased to a larger extent in controls than in type 2 diabetes. Only the controls re-gained baseline resting heart rate after 4 hours (Fig. 3a).
From baseline-1 to baseline-2, systolic blood pressure decreased in type 2 diabetes, but not in controls. Within 2 hours after fast food, the mean systolic blood pressure in the type 2 diabetes group decreased and subsequently reversed within 4 hours post-meal. In contrast, systolic blood pressure in the controls did not change after ingestion of fast food ingestion (Fig. 3b).
Overall, RPP was higher in the type 2 diabetes group versus to controls (baseline-1 and 4 hours, p < 0.01; baseline 2 and 2 hours: p < 0.05; 30 minutes, p = 0.05). The RPP was increased post-meal in both controls and type 2 diabetes (p < 0.01 and p < 0.05, respectively). It subsequently reduced within 2 hours (p < 0.01 and p < 0.05, respectively), but was changed back to baseline 2 levels after 4 hours only in the controls (Fig. 3d).
Pre- exercise did not influence heart rate, blood pressure response or RPP (Fig. 3e-h).
Biochemistry
The response of circulating glucose, C-peptide, triglycerides and TAS to fast food is illustrated in Fig. 4a-d, respectively. Fast food increased the glucose levels within 30 minutes after the meal in both groups. The subsequent drop in mean glucose levels was delayed in the type 2 diabetes group versus the control group. This was indicated by the fact that the difference 2 hours versus 30 minutes post-meal is significant for controls (p < 0.001) but not for type 2 diabetes group (p = 0.5)— only the controls returned to baseline glucose levels 4 hours post-meal (Fig. 4a). Concurrently, C-peptide levels peaked at 30 minutes post-meal in controls versus at 2 hours post-meal in the type 2 diabetes group (Fig. 4b).
The type 2 diabetes group had indications of an overall higher triglyceride level than the controls (p < 0.05, Fig. 4c). The effect of fast food on triglyceride levels was similar in both groups.
The TAS response to fast food was similar for the two groups—TAS decreased within 4 hours in both controls and type 2 diabetes (p < 0.01 and p < 0.05, respectively; Fig. 4d). Hs-CRP, HDL and LDL did not change in the postprandial phase in either group.
Discussion
Our findings indicate that fast-food induces greater overall cardiac workload in type 2 diabetes individuals than in BMI and age matched controls. Pre-exercise did not modify fast food induced changes in LV function, resting heart rate, blood pressure, blood glucose, triglycerides or total antioxidant status.
The observed postprandial increase in diastolic workload in both type 2 diabetes and healthy overweight individuals is novel. Our data contrast the few previous studies that investigated the effects of lipid infusions or a carbohydrate rich meal on cardiac function [9], [10]. Further study is needed to determine whether this is a result of the “combined meal” used here. The other studies [9], [10] might also have missed an initial increase in diastolic workload due to measuring postprandial response 1 or 2 hours after infusion or ingestion, respectively. In contrast to our finding of increased diastolic workload (e’) after the meal, von Bibra et al. [9] observed a significantly reduced diastolic workload (e’) 2 hours after ingesting a pure carbohydrate meal (48 g). Nielsen et al. [22] found no changes in diastolic function after short-term hyperglycemia by insulin discontinuation in insulin dependent type 2 diabetes individuals. However, these participants [9], [22] had longer history of type 2 diabetes and were insulin dependent.
The present study indicates that fast food interacts with LV diastolic function to a greater extent in type 2 diabetes individuals compared to controls. This could be explained by the prolonged postprandial increase in heart rate in the type 2 diabetes group: An increased heart rate increases diastolic function (E, e’) and shortens IVRT. The decrease in filling pressure in the type 2 diabetes group within 2 h post-meal, could be explained by the indication of sustained increase in e’ at this time point in this group while E is reduced.
We could speculate whether the postprandial diastolic compensations observed in the type 2 diabetes group is an early sign of diastolic dysfunction. However, further research is needed to investigate the progress and interaction of food ingestion and diastolic compensations in type 2 diabetes across different disease stages.
The increased LV systolic workload after fast food ingestion is in line with Holland et al. [10] who demonstrated increased systolic workload (LV global strain rate) induced by increased circulating triglycerides after intra venous administration of a fat emulsion in healthy individuals, and Nielsen et al. [22] who observed increased systolic workload (S’ and strain rate) due to hyperglycemia in type 2 diabetes individuals with and without heart failure. However, our data is in contrast to von Bibra et al. [9] who observed no postprandial change in systolic function (S’) in insulin dependent type 2 diabetes individuals with longer duration after ingesting carbohydrates. The diverse findings may be due to different measurement times as well as differences in methods used to increase circulating glucose and/or triglycerides.
The RPP differences seen here between groups suggest that the type 2 diabetes group had greater cardiac workload compared to controls.
The higher heart rate at rest and prolonged increases in heart rate after fast food consumption by type 2 diabetes individuals relative to controls may be due to several factors including cardiovascular autonomic neuropathy (CAN) that can cause abnormalities in heart rate control by reduced vagal activity and/or high sympathetic activity [23]. Furthermore, both glucose ingestion [24] and elevated plasma fatty acid concentrations [25] may stimulate the cardiac autonomic nervous system with a possible increase in catecholamines. Thus, the effects of fast food seen here may be due to catecholamine induced increases in inotropy that result in increased contractility of the cardiac muscle as well as increased dromotropic and chronotropic effects that increases the heart rate.
Although increased heart rate is commonly observed during euglycemic clamp in this patient group as well as those with metabolic syndrome [23], von Bibra et al. [9] observed no particular increase in resting heart rate 2 hours after a carbohydrate-rich meal in insulin dependent type 2 diabetes individuals. This may be due to the long standing type 2 diabetes [9], which increase the possibility of depressed sympathetic activity [23]. Nielsen et al. [26] observed a tendency towards increased heart rate (p = 0.08) due to high levels of lipid infusion versus low lipid infusion controls—this indicates that fast food may increase heart rate more than healthy foods.
The postprandial reduction in systolic blood pressure in the type 2 diabetes group might be an early stage of postprandial systolic hypotension, which is a common hemodynamic condition in diabetes [27] and is associated with an increased risk of cerebrovascular disease [28]. The mechanisms mediating postprandial reductions in blood pressure are not fully understood, but food-induced neurohormonal changes leading to reduced vascular resistance in the splanchnic vasculature as well as CAN, resulting in impaired sympathetic nervous activity has been suggested [29]–[31].
Gudmundsdottir et al. [32] investigated the postprandial changes after a healthy meal versus a fast food meal and found small changes in blood lipids and hs-CRP with no differences between meals. Our study supports these findings with no changes in cholesterol and hs-CRP.
In the present study, pre-exercise did not modify TAS in type 2 diabetes or controls. This is in contrast to Tyldum et al. [8] who observed a significant exercise-induced improvement in TAS, associated with improvements in endothelial function in healthy normal weight men (42 ± 4 years) using the same protocol as described here. This indicates that our participants had a poorer response to exercise versus lean and healthy individuals [8]. This may possibly be due to central obesity and poorer metabolic control in our study participants versus normal weight individuals.
The lack of exercise-induced improvements in postprandial TAS in the present study may be explained by a lack of exercise induced postprandial changes in circulating glucose- and triglyceride levels. Although the lack of exercise-induced TAS changes contrast with the findings of Tyldum et al. [8], the lack of exercise induced changes in glucose- and triglyceride levels did concur. Nevertheless, exercise-induced changes have previously been observed due to acute exercise on postprandial triglyceride levels and hyperglycemia [33]–[35].
However, studies are difficult to compare due to different measurement methods, meal composition and size, timing of exercise, exercise mode, intensity and duration. Inadequate energy expenditure [36] and/or inadequate exercise timing relative to the meal may explain the lack of exercise induced reduction in postprandial glucose [37] – and/or triglyceride excursion [38], etc. The acute effect of different exercise modes and timing of these on the postprandial response of the LV certainly needs to be further investigated in type 2 diabetes as the time course of adaptation may be different in the heart/endothelium than normal body weight persons.
Conclusions
Our findings indicate that fast food induces greater and sustained overall cardiac workload in the postprandial phase in type 2 diabetes individuals compared to BMI and age matched controls. Pre-exercise had no acute effects to the postprandial phase. The acute interaction of food on cardiac function in type 2 diabetes needs further study. More research is also needed on the effects of other exercise methods and exercise timing on postprandial cardiac function and other cardiovascular risk markers in this patient group.
Pre-exercise did not influence any biochemical variables measured at any time-point (Fig. 4e-h).

Conclusions
Our findings indicate that fast food induces greater and sustained overall cardiac workload in the postprandial phase in type 2 diabetes individuals compared to BMI and age matched controls. Pre-exercise had no acute effects to the postprandial phase. The acute interaction of food on cardiac function in type 2 diabetes needs further study. More research is also needed on the effects of other exercise methods and exercise timing on postprandial cardiac function and other cardiovascular risk markers in this patient group.
Limitations
The limitations of this study include a small sample size and similarity (BMI and WC) between groups. We evaluated the effect of fast-food on LV function, and therefore the individual effects of carbohydrates, fat and salt cannot be evaluated. A recent study demonstrated no effect on diastolic function in normotensive healthy men after one week of high dietary sodium intake [39]. However a previous study found that one week of high dietary sodium intake impair myocardial relaxation [40]. The strengths of this study include the strictly controlled study environment, supervised exercise interventions as well as the similarity in BMI and WC between groups as it excludes potentially confounding effects of adiposity.
Competing interest
The authors declare that they have no competing interests.
Authors’ contributions
SMH designed the protocol, retrieved funding, administrated the project, collected- and interpreted data and wrote the manuscript; VM collected data, contributed to the discussion and reviewed the manuscript; TF performed the statistical analyses, contributed to the discussion and reviewed the manuscript; UW supervised the project, contributed to the discussion and interpretation of data and edited the manuscript; CBI supervised the project, retrieved funding, designed the protocol, collected and interpreted data, reviewed and edited the manuscript and collected data. All authors read and approved the final manuscript.
Statement of assistance
The authors acknowledge the echocardiographic assistance of colleagues at the St. Olavs Hospital and Norwegian University of Science and Technology, Trondheim, Norway: Torfinn Eriksen, Bjørn Olav Haugen, Ola Kleveland, Erik Madsen, Tomas Renhult Skaug and Asbjørn Støylen, as well as the research assistance of Bjarne Nes and Arnt Erik Tjønna, Nina Backlund and Gøril Bakken Rønning.
Guarantors
C.B.I and S.M.H are equal guarantors taking responsibility of the contents of the article.
Funding
The study was funded by the Liaison Committee between the Central Norway Regional Health Authority (RHA) and the Norwegian University of Science and Technology (NTNU), K.G. Jebsen Foundation for Medical Research and the Norwegian Diabetes Association.

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