Responses of gut microbiota and glucose and lipid metabolism to prebiotics in genetic obese and diet-induced leptin-resistant mice

Diabetes. 2011 Nov;60(11):2775-86. doi: 10.2337/db11-0227. Epub 2011 Sep 20.

Abstract

Objective: To investigate deep and comprehensive analysis of gut microbial communities and biological parameters after prebiotic administration in obese and diabetic mice.

Research design and methods: Genetic (ob/ob) or diet-induced obese and diabetic mice were chronically fed with prebiotic-enriched diet or with a control diet. Extensive gut microbiota analyses, including quantitative PCR, pyrosequencing of the 16S rRNA, and phylogenetic microarrays, were performed in ob/ob mice. The impact of gut microbiota modulation on leptin sensitivity was investigated in diet-induced leptin-resistant mice. Metabolic parameters, gene expression, glucose homeostasis, and enteroendocrine-related L-cell function were documented in both models.

Results: In ob/ob mice, prebiotic feeding decreased Firmicutes and increased Bacteroidetes phyla, but also changed 102 distinct taxa, 16 of which displayed a >10-fold change in abundance. In addition, prebiotics improved glucose tolerance, increased L-cell number and associated parameters (intestinal proglucagon mRNA expression and plasma glucagon-like peptide-1 levels), and reduced fat-mass development, oxidative stress, and low-grade inflammation. In high fat-fed mice, prebiotic treatment improved leptin sensitivity as well as metabolic parameters.

Conclusions: We conclude that specific gut microbiota modulation improves glucose homeostasis, leptin sensitivity, and target enteroendocrine cell activity in obese and diabetic mice. By profiling the gut microbiota, we identified a catalog of putative bacterial targets that may affect host metabolism in obesity and diabetes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cecum / microbiology*
  • Colon / metabolism
  • Colon / pathology
  • Diabetes Mellitus, Type 2 / blood
  • Diabetes Mellitus, Type 2 / diet therapy*
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / pathology
  • Dietary Fats / adverse effects
  • Enteroendocrine Cells / metabolism
  • Enteroendocrine Cells / pathology
  • Gene Expression Regulation
  • Glucagon-Like Peptide 1 / blood
  • Glucose Intolerance / prevention & control
  • Gram-Negative Bacteria / classification
  • Gram-Negative Bacteria / isolation & purification
  • Gram-Positive Bacteria / classification
  • Gram-Positive Bacteria / isolation & purification
  • Hyperglycemia / prevention & control*
  • Hyperlipidemias / prevention & control*
  • Leptin / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • Molecular Typing
  • Obesity / blood
  • Obesity / diet therapy*
  • Obesity / metabolism
  • Obesity / pathology
  • Prebiotics*
  • Proglucagon / genetics
  • Proglucagon / metabolism
  • RNA, Messenger / metabolism

Substances

  • Dietary Fats
  • Leptin
  • Prebiotics
  • RNA, Messenger
  • Proglucagon
  • Glucagon-Like Peptide 1