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Gut Microbes. 2014 Jul 1;5(4):544-51. doi: 10.4161/gmic.29331. Epub 2014 Jul 8.

Intestinal microbiota in metabolic diseases: from bacterial community structure and functions to species of pathophysiological relevance.

Author information

1
Junior Research Group Intestinal Microbiome; ZIEL-Research Center for Nutrition and Food Sciences; Technische Universität München; Freising-Weihenstephan, Germany.
2
Molecular Nutrition Unit; ZIEL-Research Center for Nutrition and Food Sciences; Technische Universität München; Freising-Weihenstephan, Germany.
3
Chair of Nutrition and Immunology; Biofunctionality Unit; ZIEL-Research Center for Nutrition and Food Sciences; Technische Universität München; Freising-Weihenstephan, Germany.
4
INRA / AgroParisTech; Micalis UMR1319; Jouy-en-Josas, France.
5
Institute of Food Chemistry; Hamburg School of Food Science; University of Hamburg; Hamburg, Germany.

Abstract

The trillions of bacterial cells that colonize the mammalian digestive tract influence both host physiology and the fate of dietary compounds. Gnotobionts and fecal transplantation have been instrumental in revealing the causal role of intestinal bacteria in energy homeostasis and metabolic dysfunctions such as type-2 diabetes. However, the exact contribution of gut bacterial metabolism to host energy balance is still unclear and knowledge about underlying molecular mechanisms is scant. We have previously characterized cecal bacterial community functions and host responses in diet-induced obese mice using omics approaches. Based on these studies, we here discuss issues on the relevance of mouse models, give evidence that the metabolism of cholesterol-derived compounds by gut bacteria is of particular importance in the context of metabolic disorders and that dominant species of the family Coriobacteriaceae are good models to study these functions.

KEYWORDS:

Coriobacteriaceae; bile acids; diabetes; high-fat diet; intestinal microbiota; metabolomics; metaproteome; mouse models; obesity; steroids

PMID:
25003516
DOI:
10.4161/gmic.29331
[Indexed for MEDLINE]

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