Our major research goal is to dissect the hypothalamic neuron-glia interactions in regulation of energy homeostasis in animal models and human, at levels of intercellular signaling and organelles functionality. Not until recently, we gained knowledge that the mechanism under the development of metabolic diseases is beyond canonical concept that brain metabolic sensing and regulation is dominated by the role of neurons. The microenvironment in which neurons live is supported and maintained by other cells. In this microenvironment, the innate immune microglial cells function as the immune homeostatic keeper, by clearance of cell debris and invading pathogens through phagocytosis, and initiating immune response. Our recent studies in obese/prediabetic animal models showed that microglial immunometabolism- and hormones- regulated phagocytosis play a key role in maintaining healthy microenvironment for neural survival and neural circuits development. In postmortem brain tissue of type 2 diabetic individuals, we discovered variety of changes in microglia in different brain regions, such as the suprachiasmatic nucleus that controls biological rhythm in physiology and behavior, and in infundibular nucleus that controls food intake and energy expenditure.  

Our main projects:

• Determine in rodents the impact of a hypercaloric environment on hypothalamic microglial function.
• Study in rodents the impact of microglial-derived factors on neuronal function.  
• Translational studies on neuron-glial interactions in the human hypothalamus. 

Our long-term goal is to search for targets in microglia and neurons in hypothalamus that can rescue neuronal dysfunction in hypercaloric environment and treat obesity and type 2 diabetes.