837 resultados para High-fat diets
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Microsomal triglyceride transfer protein (MTP) is a protein that exerts a central regulatory role in very-low-density lipoprotein (VLDL) assembly and secretion. The purpose of the study was to investigate the effects of all exercise-training program oil hepatic content of MTP and its relation to hepatic VLDL-triglyceride (VLDL-TG) production in response to lipid infusion. Female rats either fed a standard (SD) or all obesity-induced high-fat (HF; 43% as energy) diet for 8 weeks were Subdivided into sedentary (Sed) and trained (Tr) groups. Exercise training consisted Of Continuous running on a motor-driven rodent treadmill 5 times/week for 8 weeks. At the end of this period, all rats in the fasted state were intravenously infused with a 20% Solution of intralipid for 3 h followed by all injection of Triton WR1339 to block lipoprotein lipase. An additional control grout) consisting of Sed rats fed the SD diet was infused with saline (0.9% NaCl). Plasma TG accumulation was thereafter measured during 90 min to estimate VLDL-TG production. Under HF diet, hepatic MTP content and plasma TG accumulation after Triton blockade (thus reflecting VLDL-TG synthesis and secretion) were not changed in Sed rats, whereas liver TG content was highly increased (similar to 90%; p<0.01). Oil the other hand, training reduced liver MTP protein content in both SD(-18%) and HF(-23%) fed rats(p<0.05). Plasma VLDL-TG accumulation was also lower (p<0.05) in Tr than in Sed rats fed the HF diet. This effect was not observed in SD fed rats. Furthermore, the exercise training-induced decrease in VLDL-TG production in HF rats was associated with a decrease in liver TG levels. It is Concluded that in addition to a reduction in liver TG content, exercise training reduces VLDL synthesis and/or secretion in HF fed rats probably via MTP regulation.
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Type 2 diabetes mellitus results from the complex association of insulin resistance and pancreatic beta-cell failure. Obesity is the main risk factor for type 2 diabetes mellitus, and recent studies have shown that, in diet-induced obesity, the hypothalamus becomes inflamed and dysfunctional, resulting in the loss of the perfect coupling between caloric intake and energy expenditure. Because pancreatic beta-cell function is, in part, under the control of the autonomic nervous system, we evaluated the role of hypothalamic inflammation in pancreatic islet function. In diet-induced obesity, the earliest markers of hypothalamic inflammation are present at 8 weeks after the beginning of the high fat diet; similarly, the loss of the first phase of insulin secretion is detected at the same time point and is restored following sympathectomy. Intracerebroventricular injection of a low dose of tumor necrosis factor a leads to a dysfunctional increase in insulin secretion and activates the expression of a number of markers of apoptosis in pancreatic islets. In addition, the injection of stearic acid intracerebroventricularly, which leads to hypothalamic inflammation through the activation of tau-like receptor-4 and endoplasmic reticulum stress, produces an impairment of insulin secretion, accompanied by increased expression of markers of apoptosis. The defective insulin secretion, in this case, is partially dependent on sympathetic signal-induced peroxisome proliferator receptor-gamma coactivator Delta a and uncoupling protein-2 expression and is restored after sympathectomy or following PGC1 alpha expression inhibition by an antisense oligonucleotide. Thus, the autonomic signals generated in concert with hypothalamic inflammation can impair pancreatic islet function, a phenomenon that may explain the early link between obesity and defective insulin secretion.
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Obesity and insulin resistance are rapidly expanding public health problems. These disturbances are related to many diseases, including heart pathology. Acting through the Akt/mTOR pathway, insulin has numerous and important physiological functions, such as the induction of growth and survival of many cell types and cardiac hypertrophy. However, obesity and insulin resistance can alter mTOR/p70S6k. Exercise training is known to induce this pathway, but never in the heart of diet-induced obesity subjects. To evaluate the effect of exercise training on mTOR/p70S6k in the heart of obese Wistar rats, we analyzed the effects of 12 weeks of swimming on obese rats, induced by a high-fat diet. Exercise training reduced epididymal fat, fasting serum insulin and plasma glucose disappearance. Western blot analyses showed that exercise training increased the ability of insulin to phosphorylate intracellular molecules such as Akt (2.3-fold) and Foxo1 (1.7-fold). Moreover, reduced activities and expressions of proteins, induced by the high-fat diet in rats, such as phospho-JNK (1.9-fold), NF-kB (1.6-fold) and PTP-1B (1.5-fold), were observed. Finally, exercise training increased the activities of the transduction pathways of insulin-dependent protein synthesis, as shown by increases in Raptor phosphorylation (1.7-fold), p70S6k phosphorylation (1.9-fold), and 4E-BP1 phosphorylation (1.4-fold) and a reduction in atrogin-1 expression (2.1-fold). Results demonstrate a pivotal regulatory role of exercise training on the Akt/ mTOR pathway, in turn, promoting protein synthesis and antagonizing protein degradation. J. Cell. Physiol. 226: 666-674, 2011. (C) 2010 Wiley-Liss, Inc.
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The present study examined the effects of aerobic training and energy restriction on adipokines levels in mesenteric (MEAT) and retroperitoneal (RPAT) white adipose tissue from obese rats. Male Wistar rats were fed with standard laboratory diet (Control group) or high fat diet (HFD). After 15 weeks, HFD rats were randomly assigned to the following groups: rats submitted to HFD, which were sedentary (sedentary HFD, n = 8) or trained (trained HFD, n = 8); or submitted to energy-restriction (ER), which were sedentary (sedentary ER, n = 8) or trained (trained ER, n = 8). Trained rats ran on a treadmill at 55% VO(2max) for 60 min/day, 5 days/week, for 10 weeks. ER rats were submitted to a reduction of 20% daily caloric ingestion compared to the Control group. ER and aerobic training decreased body weight, MEAT and RPAT absolute weight, and fat mass. IL-6, IL-10 and TNF-alpha levels were decreased and adiponectin did not change in RPAT in response to ER protocol. On the other hand, ER and the aerobic training protocol decreased IL-6, TNF-alpha and adiponectin levels in MEAT. Absolute MEAT weight showed a positive correlation with IL-6 (r = 0.464), INF-alpha (r = 0.508); and adiponectin (r = 0.342). These results suggest a tissue-specific heterogeneous response in adipokines level. The combination of the protocols (aerobic training and energy restriction) did not induce an enhanced effect. Published by Elsevier Ltd.
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Objetivou-se avaliar a substituição do milho em grão pela polpa cítrica peletizada e seus efeitos sobre os ganhos de peso, as taxas de deposição e a composição química corporal de tourinhos Santa Gertrudes em confinamento. Vinte e oito animais (idade média de nove meses e peso inicial de 277 kg) foram mantidos em baias individuais durante 92 dias, após 21 dias de adaptação. Os animais receberam dietas contendo 20% da MS como silagem de milho que continha 40% de grãos. Foram testados os níveis de 0, 25, 40 e 55% de participação da polpa cítrica peletizada na MS da dieta. A composição química corporal foi estimada a partir de equações desenvolvidas para a mesma raça, utilizando-se a composição química do corte da 9-10-11ª costelas. A participação da polpa cítrica peletizada não afetou significativamente o peso corporal final (449 kg) e os ganhos diários de peso corporal (1,50 kg), de corpo vazio (1,26 kg) e de carcaça (0,78 kg). Não houve diferença entre tratamentos para as taxas diárias de deposição de água (0,374 kg), EE (0,589 kg), proteína (0,253 kg), minerais (0,040 kg) e energia (6,934 Mcal) e, conseqüentemente, a composição química corporal final foi similar entre os animais recebendo diferentes níveis de polpa cítrica na dieta. A substituição do milho em grão por polpa cítrica peletizada, até 55% da MS, em dietas para tourinhos em terminação recebendo altos níveis de concentrado, não altera os ganhos de peso, as taxas de deposição e a composição química corporal desses animais.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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OBJETIVO: Analisar os efeitos de diferentes níveis de triglicerídeos fornecidos pela dieta sobre os parâmetros séricos triglicerídeos e lipoproteínas de alta densidade e o peso corporal de ratos sedentários e exercitados. MÉTODOS: Foram utilizados ratos Wistar, alimentados com dietas controle (7%peso/peso) e hiperlipídica (14% peso/peso) e subdivididos em sedentários e exercitados, por um período de 8 semanas. RESULTADOS: Verificou-se que o peso não diferiu entre os grupos, embora o consumo tenha sido reduzido nos grupos com dieta hiperlipídica. Os níveis de triglicerídeos não foram aumentados com a dieta rica em gordura e o HDL-colesterol se elevou apenas entre os animais exercitados que tiveram dieta normolipídica. CONCLUSÃO: A intensidade e o tempo de exercício físico influenciam de maneira mais aguda os níveis de HDL-colesterol em comparação aos níveis de triglicérides. Sugere-se que a dieta hiperlipídica deveria sobrepor (14%peso/peso) de gordura para que houvesse alterações relevantes nos parâmetros lipídicos e supostamente um aumento da performance física.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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OBJETIVO: Revisar estudos que abordam as práticas alimentares atuais e o padrão de atividade física como contribuintes do excesso de peso na infância. FONTES DE DADOS: Ovid Journals, Highwire e SciELO, com seleção de artigos originais e de revisão nos últimos dez anos (1997 a 2007), na língua portuguesa e inglesa. SÍNTESE DE DADOS: O acompanhamento do estado nutricional de crianças permite diagnosticar seu estado de saúde atual, bem como predizer parcialmente seu prognóstico na vida adulta. A prevalência de obesidade infantil, no Brasil, apresenta aumento progressivo em todas as classes sociais e sua freqüência varia entre cinco a 18%, dependendo da região estudada. A associação da transição epidemiológica, demográfica e comportamental e a alteração do hábito alimentar são apontadas como fatores causais do aumento progressivo da obesidade infantil. Práticas alimentares caracterizadas por elevado teor de lipídios, sacarose e sódio e por reduzido consumo de cereais integrais, frutas e hortaliças associadas à inatividade física decorrente do uso de computadores, jogos eletrônicos e televisores influenciam parte considerável de crianças. Este estilo de vida reflete os hábitos familiares e pode ser influenciado pelo ambiente escolar no qual a criança está inserida. CONCLUSÕES: Os dados sugerem influência considerável dos fatores ambientais, principalmente hábitos alimentares e inatividade física, no crescente aumento da prevalência de excesso de peso na população pediátrica.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)