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

Curr Opin Clin Nutr Metab Care. 2011 Jul;14(4):328-33. doi: 10.1097/MCO.0b013e3283478727.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adipose Tissue / metabolism
  • Animals
  • Biomarkers / metabolism
  • Colitis / pathology
  • Cytokines / metabolism
  • Diet
  • Dietary Fats / adverse effects
  • Humans
  • Inflammation / complications*
  • Inflammation / microbiology
  • Insulin Resistance*
  • Intestinal Mucosa / metabolism
  • Intestines / microbiology
  • Intestines / pathology*
  • Lipopolysaccharides / metabolism
  • Models, Animal
  • Obesity / complications
  • Obesity / microbiology
  • Obesity / pathology*
  • Toll-Like Receptor 5 / metabolism


  • Biomarkers
  • Cytokines
  • Dietary Fats
  • Lipopolysaccharides
  • Toll-Like Receptor 5