GLP-1R signaling modulates colonic energy metabolism, goblet cell number and survival in the absence of gut microbiota.

ABSTRACT:

Objectives

Gut microbiota increases energy availability through fermentation of dietary fibers to short-chain fatty acids in conventionally raised mice. Energy deficiency in germ-free (GF) mice increases glucagon-like peptide-1 (GLP-1) levels, which slows intestinal transit. To further analyze the role of GLP-1-mediated signaling in this model of energy deficiency, we re-derived mice lacking GLP-1 receptor (GLP-1R KO) as GF.

Methods

GLP-1R KO mice were rederived as GF through hysterectomy and monitored for 30 weeks. Mice were subjected to rescue experiments either through feeding an energy-rich diet or colonization with a normal cecal microbiota. Histology and intestinal function were assessed at different ages. Intestinal organoids were assessed to investigate stemness.

SUBMITTER: Greiner TU 

PROVIDER: S-EPMC11002751 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature