Gut commensal Bacteroides acidifaciens prevents obesity and improves insulin sensitivity in mice

Mucosal Immunol. 2017 Jan;10(1):104-116. doi: 10.1038/mi.2016.42. Epub 2016 Apr 27.

Abstract

In humans, the composition of gut commensal bacteria is closely correlated with obesity. The bacteria modulate metabolites and influence host immunity. In this study, we attempted to determine whether there is a direct correlation between specific commensal bacteria and host metabolism. As mice aged, we found significantly reduced body weight and fat mass in Atg7ΔCD11c mice when compared with Atg7f/f mice. When mice shared commensal bacteria by co-housing or feces transfer experiments, body weight and fat mass were similar in both mouse groups. By pyrosequencing analysis, Bacteroides acidifaciens (BA) was significantly increased in feces of Atg7ΔCD11c mice compared with those of control Atg7f/f mice. Wild-type C57BL/6 (B6) mice fed with BA were significantly more likely to gain less weight and fat mass than mice fed with PBS. Of note, the expression level of peroxisome proliferator-activated receptor alpha (PPARα) was consistently increased in the adipose tissues of Atg7ΔCD11c mice, B6 mice transferred with fecal microbiota of Atg7ΔCD11c mice, and BA-fed B6 mice. Furthermore, B6 mice fed with BA showed elevated insulin levels in serum, accompanied by increased serum glucagon-like peptide-1 and decreased intestinal dipeptidyl peptidase-4. These finding suggest that BA may have potential for treatment of metabolic diseases such as diabetes and obesity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / microbiology
  • Adipose Tissue / physiology*
  • Animals
  • Autophagy-Related Protein 7 / genetics
  • Bacteroides / immunology*
  • Cells, Cultured
  • Dipeptidyl Peptidase 4 / genetics
  • Dipeptidyl Peptidase 4 / metabolism
  • Feces / microbiology
  • Gastrointestinal Microbiome / immunology*
  • Gene Expression Regulation
  • Glucagon-Like Peptide 1 / blood
  • Humans
  • Insulin / blood
  • Insulin Resistance / immunology*
  • Intestines / microbiology
  • Intestines / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Obesity / immunology
  • Obesity / microbiology*
  • PPAR alpha / genetics
  • PPAR alpha / metabolism
  • Symbiosis

Substances

  • Atg7 protein, mouse
  • Insulin
  • PPAR alpha
  • Glucagon-Like Peptide 1
  • Dipeptidyl Peptidase 4
  • Autophagy-Related Protein 7