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Review
. 2011 Jul;14(4):328-33.
doi: 10.1097/MCO.0b013e3283478727.

Role of intestinal inflammation as an early event in obesity and insulin resistance

Shengli Ding  1 , Pauline K Lund
Affiliations
Review

Role of intestinal inflammation as an early event in obesity and insulin resistance

Shengli Ding et al. Curr Opin Clin Nutr Metab Care. 2011 Jul.

Abstract

Purpose of review: To highlight recent evidence supporting a concept that intestinal inflammation is a mediator or contributor to development of obesity and insulin resistance.

Recent findings: Current views suggest that obesity-associated systemic and adipose tissue inflammation promote insulin resistance, which underlies many obesity-linked health risks. Diet-induced changes in gut microbiota also contribute to obesity. Recent findings support a concept that high-fat diet and bacteria interact to promote early inflammatory changes in the small intestine that contribute to development of or susceptibility to obesity and insulin resistance. This review summarizes the evidence supporting a role of intestinal inflammation in diet-induced obesity and insulin resistance and discusses mechanisms.

Summary: The role of diet-induced intestinal inflammation as an early biomarker and mediator of obesity, and insulin resistance warrants further study.

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Figures

Figure 1
Figure 1. Mechanisms of insulin resistance linked to proinflammatory cytokines
Insulin activation of insulin receptor (IR) normally promotes tyrosine phosphorylation of IRS-1 (or IRS-2) to mediate downstream signaling. Proinflammatory cytokines block insulin/insulin receptor action by inducing suppressors of cytokine signaling (SOCS), which prevent IRS-1 binding to IR and by promoting serine phosphorylation and inactivation of IRS-1 via proinflammatory Jun-Kinase or NFκB pathways.
Figure 2
Figure 2. Proposed roles of intestinal inflammation in obesity and insulin resistance
Top: current views of diet-associated obesity linking diet and gut microbes to development of obesity, and subsequent systemic or adipose inflammation promoting insulin resistance. Bottom: proposed, although not mutually exclusive, model of mechanism by which diet interactions with gut microbes or metabolites induces early proinflammatory changes in the intestine which, by the multiple mechanisms indicated, promote or increase susceptibility to obesity and insulin resistance.
See this image and copyright information in PMC

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