Gut microbiota as a regulator of energy homeostasis and ectopic fat deposition: mechanisms and implications for metabolic disorders

Curr Opin Lipidol. 2010 Feb;21(1):76-83. doi: 10.1097/MOL.0b013e3283347ebb.

Abstract

Purpose of review: To examine the role of gut microbiota in the regulation of host energy homeostasis and its role in the pathogenesis of obesity, diabetes and nonalcoholic fatty liver disease (NAFLD).

Recent findings: Experimental models highlight several mechanisms connecting gut microbiota to host energy metabolism: increased energy harvesting from the diet, regulation of appetite through gut peptide, secretion, regulation of tissue-free fatty acid composition and uptake, storage and oxidation, modulation of intestinal barrier by glucagon-like peptide-2 secretion, activation of innate immunity and hepatic fibrogenesis through the lipopolysaccharide (LPS)-toll-like receptor-4 axis.Gut microbiota manipulation through antibiotics, prebiotics and probiotics yields encouraging results for the treatment of obesity, diabetes and NAFLD in animal models, but data in humans are currently scarce.

Summary: Gut microbiota manipulation yielded encouraging results for the treatment of different metabolic disorders in experimental models. However, changing intestinal microbiota may be more difficult in free-living individuals compared to standardized laboratory models, and its long-term consequences are unknown. To safely and effectively change human gut microflora, future research should highlight the complex hormonal, immunomodulatory and metabolic mechanisms underlying microbiota-host interactions in different tissues and candidate treatments should be evaluated in well designed trials with patient-oriented end-points.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Digestive System / metabolism
  • Digestive System / microbiology*
  • Energy Metabolism*
  • Fatty Acids / metabolism*
  • Homeostasis*
  • Humans
  • Metabolic Diseases / metabolism*
  • Metabolic Diseases / microbiology*
  • Metagenome / physiology*

Substances

  • Fatty Acids