Postdoc position in energy homeostasis (Microglial Biology)

Regulation of energy homeostasis is key for organisms to cope with changes in food availability. NPY/AgRP and POMC neurons in the arcuate nucleus of the hypothalamus emerged as major control points translating hormonal inputs into alterations in feeding behavior and energy metabolism. Dysregulation of this intricate system contributes to obesity and type 2 diabetes (T2D). Using conditional knockout mice, we identified CaMK1D – encoded by a gene located in one of the established risk loci associated with T2D – to be required in neuronal control of food intake in response to ghrelin. We have unveiled a specific function of CaMK1D in AgRP neurons in response to ghrelin and fasting using state-of-the-art stereotactic and chemogenetic tools. Interestingly, we also recently found that deletion of CaMK1D in the microglia had an impact on food intake and energy metabolism. In fact, activation of microglial cells in the course of obesity is emerging as a pivotal mechanism impairing food intake control. Based on these preliminary findings, we propose innovative strategies to identify a precise CaMK1D-dependent inflammatory mechanism emerging from microglial cells that potentially impacts on neuronal regulation of energy homeostasis.