Western lifestyle has transformed obesity into an alarming epidemic. Of particular concern are the concurrent and parallel increases in the prevalence of pathological conditions associated with obesity, such as insulin resistance, type 2 diabetes and cardiovascular disease. The pathophysiology of obesity-induced insulin resistance is attributable to the ectopic deposition of fat in liver, muscle and pancreas, and the increase in adipose tissue inflammation.
Our group is interested in the molecular mechanisms implicated in the pathogenesis of obesity and type 2 diabetes. In particular, we study the role of fatty acids in metabolism, focusing on Carnitine Palmitoyltransferase I (CPTI), the key regulatory enzyme in mitochondrial fatty-acid oxidation. CPTI catalyses the rate-limiting step in the entry of cytosolic long-chain acyl-CoA into mitochondria, where β-oxidation takes place. There are three isoforms of CPTI: CPTIA, mainly expressed in liver and pancreas; CPTIB, expressed in skeletal muscle; and CPTIC, expressed in the brain.
Our research lines include the study of fatty-acid metabolism in: 1) Obesity-induced insulin resistance and type 2 diabetes (pancreas, muscle, liver and adipose tissue); 2) Appetite (hypothalamus); and 3) Development of potential new treatments for obesity and type 2 diabetes, through structural studies of CPTI-related drugs.