Abstract
Obesity results from alterations in the body’s regulation of energy intake, expenditure, and storage. Animal and human data demonstrate that phylogenic changes occur in the microbiota composition in obese individuals. Furthermore, evidence from animal models suggest that the alterations of the gut microbiota with obesity results in increased energy extraction and lipid deposition, altered release of entero-hormones, increased intestinal permeability and metabolic endotoxemia. Treatment with pre- and probiotics may reverse many of metabolic effects linked with the altered microbiota in obese patients. The gut microbiota is, therefore, a potential nutritional and pharmacological target for the management of obesity and obesity-related disorders.
Highlights
Obesity results from alterations in the body’s regulation of energy intake, expenditure, and storage
It has been shown that a diet rich in inulin and related fibers promote an increase in bifidobacteria, whereas the intake of dietary sulfate favors several genera of sulfate-reducing bacteria over methanogenic Archaea
On the basis that obesity and insulin resistance is associated with low-grade chronic systemic inflammation, Cani et al (2007a) postulated another mechanism linking the intestinal microbiota to the development of obesity. They hypothesized that bacterial lipopolysaccharide (LPS) derived from Gram-negative bacteria residing in the gut microbiota acts as a triggering factor linking inflammation to a high-fat diet-induced metabolic syndrome
Summary
Obesity results from alterations in the body’s regulation of energy intake, expenditure, and storage. The authors proposed that the gut microbiota promotes intestinal monosaccharides absorption, energy extraction from non-digestible food components via SCFA production through fermentation, de novo hepatic lipogenesis and adipocyte fatty acid storage.
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