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Abstract
Antibiotic-induced microbiome depletion (AIMD) has been used frequently to study the role of the gut microbiome in pathological conditions. However, unlike germ-free mice, the effects of AIMD on host metabolism remain incompletely understood. Here we show the effects of AIMD to elucidate its effects on gut homeostasis, luminal signaling, and metabolism. We demonstrate that AIMD, which decreases luminal Firmicutes and Bacteroidetes species, decreases baseline serum glucose levels, reduces glucose surge in a tolerance test, and improves insulin sensitivity without altering adiposity. These changes occur in the setting of decreased luminal short-chain fatty acids (SCFAs), especially butyrate, and the secondary bile acid pool, which affects whole-body bile acid metabolism. In mice, AIMD alters cecal gene expression and gut glucagon-like peptide 1 signaling. Extensive tissue remodeling and decreased availability of SCFAs shift colonocyte metabolism toward glucose utilization. We suggest that AIMD alters glucose homeostasis by potentially shifting colonocyte energy utilization from SCFAs to glucose.
Highlights
Antibiotic-induced microbiome depletion (AIMD) has been used frequently to study the role of the gut microbiome in pathological conditions
Antibiotic-induced microbiome-depleted (AIMD) mice, where luminal bacteria are reduced with the administration of four or more broad-spectrum antibiotics through gavage or drinking water, have been used in conjunction with, or sometimes instead of, germ-free (GF) mice to investigate the role of the gut microbiome in some pathological conditions[1,2,3]
We aim to investigate the effects of microbiome depletion on metabolism by performing AIMD in normal-chow fed, wild-type mice to understand its effects on host metabolism
Summary
Antibiotic-induced microbiome depletion (AIMD) has been used frequently to study the role of the gut microbiome in pathological conditions. We demonstrate that AIMD, which decreases luminal Firmicutes and Bacteroidetes species, decreases baseline serum glucose levels, reduces glucose surge in a tolerance test, and improves insulin sensitivity without altering adiposity. These changes occur in the setting of decreased luminal short-chain fatty acids (SCFAs), especially butyrate, and the secondary bile acid pool, which affects whole-body bile acid metabolism. The metabolic effects of the absence of microbiota in GF mice have been well characterized—for example, change in the luminal and serum bile acid (BA) pool, increased incretin release, decreased short-chain fatty acid (SCFA) availability, and altered glucose homeostasis[4,5,6]. Since AIMD reduces bacteria with BSH, it could have a protective effect and improve insulin sensitivity
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