B.R.A.I.N.E.D Team : Brain Regulation Across Integrated Neural Energy Dynamics

Why do we eat? The question seems simple. Yet the molecular mechanisms that regulate hunger, satiety and energy expenditure are remarkably complex. Exploring this interface between neurobiology and metabolism drives our research on a daily basis. This work goes beyond scientific curiosity. In a world where obesity and type 2 diabetes affect hundreds of millions of people, it has become a necessity.
In this context, CaMK1D drew our attention. Long associated with peripheral functions, this kinase in fact plays an unsuspected central role that our work was the first to uncover. Conditional deletion of CaMK1D in mice profoundly disrupts energy homeostasis and notably confers resistance to diet-induced obesity. An unexpected finding that reveals a major role in the adaptation to nutritional excess.
Today, our team is dedicated to deciphering the molecular mechanisms that position CaMK1D as a key actor within the circuits controlling food intake and energy expenditure. We combine molecular approaches, cellular analyses and metabolic phenotyping to identify the signaling pathways involved. As our work progresses, new questions emerge, involving other kinases, other cell types and other forms of energy homeostasis dysregulation.
Many questions remain. Yet the outlines of a new model of energy regulation are beginning to emerge. This is precisely the challenge that the B.R.A.I.N.E.D team is committed to tackling by deciphering the fundamental mechanisms that govern energy balance.