Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/320355
Type: Artigo de Periódico
Title: Linking Gut Microbiota And Inflammation To Obesity And Insulin Resistance
Author: Saad
MJA; Santos
A; Prada
PO
Abstract: Obesity and insulin resistance are the major predisposing factors to comorbidities, such as Type 2 diabetes, nonalcoholic fatty liver disease, cardiovascular and neurodegenerative diseases, and several types of cancer. The prevalence of obesity is still increasing worldwide and now affects a large number of individuals. Here, we review the role of the gut microbiota in the pathophysiology of insulin resistance/obesity. The human intestine is colonized by similar to 100 trillion bacteria, which constitute the gut microbiota. Studies have shown that lean and overweight rodents and humans may present differences in the composition of their intestinal flora. Over the past 10 years, data from different sources have established a causal link between the intestinal microbiota and obesity/insulin resistance. It is important to emphasize that diet-induced obesity promotes insulin resistance by mechanisms independent and dependent on gut microbiota. In this review, we present several mechanisms that contribute to explaining the link between intestinal flora and insulin resistance/obesity. The LPS from intestinal flora bacteria can induce a chronic subclinical inflammatory process and obesity, leading to insulin resistance through activation of TLR4. The reduction in circulating SCFA may also have an essential role in the installation of reduced insulin sensitivity and obesity. Other mechanisms include effects of bile acids, branched-chain amino acids (BCAA), and some other lesser-known factors. In the near future, this area should open new therapeutic avenues for obesity/insulin resistance and its comorbidities.
Subject: Diet-induced Obesity
Necrosis-factor-alpha
Human Large-intestine
Chain Fatty-acids
Activated Protein-kinase
Type-2 Diabetes-mellitus
Human Adipose-tissue
Kappa-b Activation
Nitric-oxide
S-nitrosation
Editor: AMER PHYSIOLOGICAL SOC
Citation: Physiology. AMER PHYSIOLOGICAL SOC, n. 31, n. 4, p. 283 - 293.
Rights: fechado
Identifier DOI: 10.1152/physiol.00041.2015
Address: http://physiologyonline.physiology.org/content/31/4/283.long
Date Issue: 2016
Appears in Collections:Unicamp - Artigos e Outros Documentos

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