About Patrice D. Cani

Professor Patrice D. Cani is researcher from the Belgian Fund for Scientific Research (FRS-FNRS), group leader in the Metabolism and Nutrition research group at the Louvain Drug Research Institute (LDRI) from the Université catholique de Louvain (UCL), Brussels, Belgium, and WELBIO (Walloon Excellence in Lifesciences and BIOtechnology) investigator. He is currently member of several international associations, he is member of the Alumni College from the Royal Belgian Academy of Sciences, and he has been elected in the board of directors of the LDRI (UCL). Patrice D. Cani has a M.Sc. in Nutrition and another M.Sc. in health Sciences, he is registered dietitian and PhD in Biomedical Sciences. His main research interests are the investigation of the role of the gut microbiota in the development of metabolic disorders, such as obesity, type 2 diabetes and low grade inflammation. More specifically, he is investigating the interactions between the gut microbiota, the host and specific biological systems such as the endocannabinoid system and the innate immune system in the context of obesity, type 2 diabetes and metabolic inflammation. Prof Cani is author and co-author of more than 110 scientific research papers published in peer-reviewed international journals, conferences and book chapters.

Gut microbiota, with its close links to metabolism and the immune system, could potentially be a factor that lies at the core of good health. This means it can be positioned at the heart of the processes that influence the risk of contracting different diseases.

In a recent paper by Perry et al., researchers describe an investigation into the putative mechanisms by which gut microbiota alterations may lead to obesity, insulin resistance, and metabolic syndrome. Authors describe increased production of acetate by altered gut microbiota in rats. They link this to activation of the parasympathetic nervous system, increased glucose-stimulated insulin secretion, higher ghrelin secretion, hyperphagia, and obesity. Thus, they point to increased acetate production as a driver of metabolic syndrome.