Young-Bum Kim 1 페이지

My research focuses on identifying the molecular mechanisms mediating the metabolic action of insulin and leptin, and the resistance to these hormones that underlies diseases such as obesity and type 2 diabetes. To identify the metabolic roles of specific molecular signals, my laboratory uses genetically engineered mouse models and cultured cell systems, in conjunction with biochemical, molecular, and physiological techniques. Using these techniques, we found that Rho-kinase regulates insulin-stimulated glucose transport and signaling via either IRS-1 serine phosphorylation or actin polymerization, and also controls energy balance by targeting leptin receptor signaling, establishing a new mechanism for the regulation of insulin and leptin action. Our recent work identified apolipoprotein J (ApoJ) as a novel anorexigenic molecule that regulates appetite and energy balance. Like leptin, ApoJ treatment causes anorexia, weight loss, and hypothalamic Stat3 activation in mice. These effects are most likely mediated by a cellular mechanism that is dependent on a physical interaction between functional leptin receptor and LRP. Our findings will expand knowledge of the mechanisms underlying insulin and leptin resistance in obesity and type 2 diabetes. We are currently working on the hypothesis that hypothalamic ApoJ→LRP signaling is necessary for the normal metabolic action of leptin on food intake and energy balance, and impaired LRP signaling leads to leptin resistance and obesity.