BackgroundStudies suggest that leucine supplementation (LS) has a therapeutic potential to prevent obesity and to promote glucose homeostasis. Furthermore, regular physical exercise is a widely accepted strategy for body weight maintenance and also for the prevention of obesity. The aim of this study was to determine the effect of chronic LS alone or combined with endurance training (ET) as potential approaches for reversing the insulin resistance and obesity induced by a high-fat diet (HFD) in rats.MethodsForty-seven rats were randomly divided into two groups. Animals were fed a control diet-low fat (n = 10) or HFD (n = 37). After 15 weeks on HFD, all rats received the control diet-low fat and were randomly divided according to treatment: reference (REF), LS, ET, and LS+ET (n = 7-8 rats per group). After 6 weeks of treatment, the animals were sacrificed and body composition, fat cell volume, and serum concentrations of total cholesterol, HDL-cholesterol, triacylglycerol, glucose, adiponectin, leptin and tumor necrosis factor-alpha (TNF-α) were analyzed.ResultsAt the end of the sixth week of treatment, there was no significant difference in body weight between the REF, LS, ET and LS+ET groups. However, ET increased lean body mass in rats (P = 0.019). In addition, ET was more effective than LS in reducing adiposity (P = 0.019), serum insulin (P = 0.022) and TNF-α (P = 0.044). Conversely, LS increased serum adiponectin (P = 0.021) levels and reduced serum total cholesterol concentration (P = 0.042).ConclusionsThe results showed that LS had no beneficial effects on insulin sensitivity or adiposity in previously obese rats. On the other hand, LS was effective in increasing adiponectin levels and in reducing total cholesterol concentration.

Certain amino acids, such as leucine (Leu) are not only substrates for protein synthesis but also are important regulators of protein metabolism. Moreover, it is known that alterations in intrauterine growth favor the development of chronic diseases in adulthood. Therefore, we investigated the role of Leu in combination with other BCAA on effects that are induced by maternal protein restriction on fetal growth. Wistar rats were divided into 4 groups according to the diet provided during pregnancy: control (C; 20% casein); V+I [5% casein + 2% L-valine (Val) + 2% L-isoleucine (Ile)]; KYT [5% casein + 1.8% L-lysine (Lys) + 1.2% L-tyrosine (Tyr) + 1% L-threonine (Thr)]; and BCAA (5% casein + 1.8% L-Leu + 1.2% L-Val + 1% L-Ile). Maternal protein restriction reduced the growth and organ weight of the offspring of dams receiving the V+I and KYT diets compared with the C group. Supplementation with BCAA reversed this growth deficit, minimizing the difference or restoring the mass of organs and carcass fat, the liver and muscle protein, and the RNA concentrations compared with newborns in the C group (P < 0.05). These effects could be explained by the activation of the mTOR signaling pathway, because phosphorylation of 4E-BP1 in the liver of offspring of the BCAA group was greater than that in the C, V+I, and KYT groups. The present results identify a critical role for Leu in association with other BCAA in the activation of the mTOR signaling pathway for the control of altered intrauterine growth induced by a maternal low-protein diet.

In vivo and in vitro studies have demonstrated that high protein diets affect both protein synthesis and regulation of several cellular processes. The role of amino acids as substrate for protein synthesis has been established in the literature. However, the mechanism by which these amino acids modulate transcription and regulate the mRNA translation via mTOR-dependent signaling pathway has yet to be fully determined. It has been verified that mTOR is a protein responsible for activating a cascade of biochemical intracellular events which result in the activation of the protein translation process. Of the aminoacids, leucine is the most effective in stimulating protein synthesis and reducing proteolysis. Therefore, it promotes a positive nitrogen balance, possibly by favoring the activation of this protein. This amino acid also directly and indirectly stimulates the synthesis and secretion of insulin, enhancing its anabolic cellular effects. Therefore, this review aimed to identify the role of leucine in protein synthesis modulation and to discuss the metabolic aspects related to this aminoacid. Uniterms:Leucine. Protein synthesis. Transcription Factors. mTOR. Translation Protein.Estudos in vivo e in vitro verificaram que dietas hiperprotéicas influenciam a síntese protéica e regulam vários processos celulares. O papel dos aminoácidos como substrato para a síntese de proteínas já está bem evidenciado na literatura, porém as formas como esses aminoácidos modulam a etapa da transcrição e regulam a tradução do RNAm, pela via de sinalização dependente da mTOR, ainda não estão totalmente esclarecidas. Tem-se verificado que a mTOR é uma proteína responsável por ativar uma cascata de eventos bioquímicos intracelulares que culminam na ativação do processo de tradução protéica. Dentre todos os aminoácidos, a leucina é a mais eficaz em estimular a síntese protéica, reduzir a proteólise e, portanto, favorecer o balanço nitrogenado positivo, possivelmente por favorecer a ativação desta proteína. Além disso, este aminoácido estimula direta e indiretamente a síntese e a secreção de insulina, e, assim, aumenta as propriedades anabólicas celulares. Nesse sentido, a presente revisão tem como objetivo identificar o papel da leucina na modulação da síntese protéica e abordar aspectos metabólicos relacionados a este aminoácido.Unitermos: Leucina. Síntese protéica. Fator de transcrição. mTOR. Tradução de proteínas. INTRODUCTIONProtein synthesis in tissue is rapidly stimulated after nutrient consumption. Insulin and aminoacids stimulate protein anabolism, acting in a posterior step of gene transcription, i.e., on protein translation. However, the mechanism by which the aminoacids stimulate protein translation has yet to be fully determined (Proud, 2002).Some studies have verified that high-protein diets stimulate protein synthesis. Some of the benefits promoted by this diet on body composition can be attributed to high consumption of branched-chain aminoacids (BCAA), which include the aminoacids leucine, valine and isoleucine (Donato...

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Animal studies show that intrauterine malnutrition may cause redistribution of blood flow in uterus, which may promote permanent changes in structure and function of some organs, which causes changes in metabolism. Furthermore, intrauterine malnutrition can affect the secretion of hormones that act on fetal growth and may lead to intrauterine growth restriction. This phenomenon can partly be explained by the hypothesis of fetal programming, which is suggested that occur a metabolic and physiological adaptation of the fetus to an adverse intrauterine condition, which can induce the development of chronic diseases in later life. In this context, researches with supplementation of branched chain amino acids (BCAA), especially leucine, have verified the ability of these nutrients to promote protein synthesis in catabolic conditions, through the activation of an intracellular biochemical pathway interceded by protein kinase Mammalian Target of Rapamycin (mTOR), which is involved in the stimulating of protein translation stage. Thus, this study evaluated the effect of BCAA supplementation in offspring subjected to maternal protein-restrict diet. To this, Wistar rats were mated with adult rats of the same race. Once was confirmed the pregnancy, the pregnants were distributed into groups according to the diet that would be provided during pregnancy: CON (20% protein); VAL/ISO (5% protein + 2% + 2% VAL/ISO), AAE (5% protein + 4% EAA) and BCAA (5% protein + 4% BCAA). The protocol adopted maternal protein restriction caused a reduction in body growth and weight of the offspring's organs. Although supplementation with VAL/ISO and AAE has not recovered the effects mediated by protein deficiency, it was found that supplementation with BCAA has reversed part of the deficit observed in the growth of the offspring, since it was effective in minimizing or even fully restoring various parameters such as organ weight, carcass fat mass and parameters indicative of nutritional protein, such as the concentrations of protein and RNA in liver and muscle. These effects may be partially explained by the stimulation induced by BCAA supplementation on the mTOR signaling pathway, considering that was verified in the liver of the offspring from dams that received this supplementation augment on the phosphorylation of this protein (P < 0,05), which is responsible for triggering a cascade of molecular events that culminate, ultimately, in increased protein synthesis. Given this, it becomes relevant to conducting research to assess long-term effects of supplementation with BCAA in offspring subjected to maternal protein-restricted diet.

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