Elsevier

Molecular Metabolism

Volume 6, Issue 11, November 2017, Pages 1371-1380
Molecular Metabolism

Original Article
Host–microbiota interaction induces bi-phasic inflammation and glucose intolerance in mice

https://doi.org/10.1016/j.molmet.2017.08.016Get rights and content
Under a Creative Commons license
open access

Highlights

  • Inflammation affects glucose tolerance in early phase of colonization of GF mice.

  • Adiposity affects glucose tolerance in delayed phase of colonization of GF mice.

  • Colonization of antibiotics treated mice show only the delayed phase of glucose impairment.

Abstract

Objective

Gut microbiota modulates adiposity and glucose metabolism in humans and mice. Here we investigated how colonization of germ-free (GF) mice affects kinetics of adiposity and glucose metabolism.

Methods

Adiposity and glucose metabolism were evaluated at different time points in ex-GF and antibiotic treated mice after colonization with gut microbiota from a conventionally raised (CONV-R) mouse. Mouse physiology, microbiome configuration, serum cytokine levels, and gene expression for inflammatory markers were performed in different tissues.

Results

Colonization resulted in a bi-phasic glucose impairment: the first phase occurring within 3 days of colonization (early phase) and the second 14–28 days after colonization (delayed phase). The early phase co-occurred with an inflammatory response and was independent of adiposity, while the delayed phase was mostly ascribed to adipose tissue expansion and inflammation. Importantly, re-colonization of antibiotic treated mice displays only the delayed phase of glucose impairment and adiposity, suggesting that the early phase may be unique to colonization of the immature GF mice gut.

Conclusions

Our results provide new insights on host–microbiota interaction during colonization of GF mice and the resulting effects on adiposity and glucose metabolism in a time resolved fashion.

Keywords

Microbiota
Germ-free
Antibiotic
Colonization
Adiposity
Glucose metabolism

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