Endocrine Abstracts

The distal gut harbours microbial communities that outnumber our own eukaryotic cells. Over the last 15 years, our work has been devoted to examine the way by which gut microbiota interacts with nutrients and host physiology. We and others have suggested that cross-talks between gut microbiota and the host cells contribute to the regulation of energy, glucose and lipid homeostasis.

We described the concept of metabolic endotoxemia (increase in plasma LPS levels) as one of the triggering factors leading to the development of the metabolic inflammation and insulin resistance. Following this discovery, we found that the major factor involved in the development of metabolic endotoxemia observed upon obesity is related to the gut barrier function.

Bacterial metabolism of nutrients in the gut is able to drive the release of bioactive compounds (including short-chain fatty acids or lipid metabolites), which interact with host cellular targets to control energy metabolism and immunity.

We found in both rodents and humans that prebiotics, administration changed gut microbiota composition and activity.

In rodents, we found that specific change in the gut microbiota composition improves glucose tolerance, via GLP-1 dependent mechanisms and gut barrier via GLP-2 dependent mechanisms. More specifically, we found that prebiotics increased L-cells number and associated parameters (intestinal proglucagon mRNA expression, plasma GLP-1 and 2 levels).

Thus, although the clear mechanisms involved in the bacteria-host interactions are still under investigation, we found that the gut microbiota control enteroendocrine functions and cell differentiation.

This work is supported by ERC Starting Grant ENIGMO 336452.

Disclosure: ERC Starting Grant ENIGMO 336452.