Obesity, type-2 diabetes and low-grade inflammation are becoming worldwide epidemic. We and others have provided evidence that the gut microbiota contribute to the control of energy homeostasis. Therefore, we have defined a novel concept, that we called the MicrObesity (microbes and obesity), devoted to decipher the specific role dysbiosis and its impact on host metabolism and energy storage.
Over the last 15 years, our work has been devoted to examine the way by which the bacteria present in the gut interact with nutrients and host biology to control obesity and associated disorders, including diabetes, inflammation and liver diseases. Recently, we discovered that the gut microbiota contribute to the development of the insulin resistance and the low grade inflammation characterizing obesity. We described the concept of metabolic endotoxemia (increase in plasma LPS levels) as triggering factor in the development of the metabolic alterations associated with obesity.
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. For instance, we found that both nutritional and genetic obesity are associated with an increased gut permeability leading to the leakage of LPS and possibly other microbiota derived factors. Although the clear mechanisms involved in the bacteria-host interactions are still under investigation, we found that the gut microbiota control enteroendocrine functions such as L-cells (producing GLP-1 and GLP-2) number and differentiation, the endocannabinoid system tone but also leptin sensitivity.
We found that selective changes in the gut microbiota composition by using prebiotics reduce metabolic endotoxemia and gut permeability via different mechanisms (e.g. GLP-2, endocannabinoid system).
Taken together, the compelling data currently published suggest that specific changes in the gut microbiota could be promoted to counteract fat mass development, diabetes and the low levels of inflammation associated with obesity.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported, however funding details are unavailable.
05 - 09 May 2012
European Society of Endocrinology