Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2014) 35 S12.3 | DOI: 10.1530/endoabs.35.S12.3

ECE2014 Symposia Gut microbiota in diabetes and obesity (3 abstracts)

Functional interactions between diet, microbiota and host: effects on intestinal architecture and host nutrient absorption

Thomas Greiner


Wallenberg Laboratory/Sahlgrenska Center for Cardiovascular and Metabolic Research, Sahlgrenska University Hospital, Gothenburg, Sweden.

The human gut is home to a vast number of bacteria, the microbiota, whose genomes complement our own set of genes. The gut microbiota functions at the intersection between host genotype and diet to modulate host physiology and metabolism, and recent data have revealed that an altered gut microbiota can contribute to obesity. The gut microbiota affects host physiology and metabolism by several mechanisms including increased energy harvest from the diet, modulation of lipid metabolism, altered endocrine function, and increased inflammatory tone. Furthermore, the microbiota influences intestinal epithelial and vascular architecture which in turn may affect nutrient absorption. The composition of the microbiota is influenced by several factors including early environmental exposures and diet.

Gut microbiota contribute to host metabolic efficiency by increasing energy availability through the fermentation of dietary fiber and production of short-chain fatty acids in the colon which are proposed to stimulate secretion of the proglucagon-derived incretin hormone GLP-1. Germ-free and antibiotic-treated mice, which have severely reduced SCFA levels, have increased basal GLP-1 levels in the plasma and increased proglucagon expression specifically in the colon. Increasing energy supply suppressed colonic proglucagon expression in GF mice suggesting that colonic L-cells sense local energy availability and regulate basal GLP-1 secretion accordingly.

Increased GLP-1 levels in GF mice did not improve the incretin response but instead slowed intestinal transit suggesting that GLP-1 have additional effects on host physiology apart from the incretin effect. Increasing colon-derived GLP-1 may be an adaptive response to insufficient energy availability in the colon that slows intestinal transit and allows for greater nutrient absorption.

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