PFKFB3 control of adipocyte-macrophage crosstalk in obesity
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Obesity is a major health problem. During obesity, fat (adipose) tissue commonly presents many immune cells (inflammation), which contributes to the development of a wide verity of chronic disease including diabetes and certain forms of cancers. Much evidence suggests that nutrient overload triggers inflammation in fat tissue. However, the precise reasons are not well understood. The PI hypothesizes that adipose PFKFB3, a gene whose product regulate nutrient metabolism, controls the development of adipose tissue inflammation. More specifically, the PI will clarify how PFKFB3 orchestrate the crosstalk between fat cells and immune cells that residing in fat tissue. Mice with selective deletion of PFKFB3 in fat cells and in immune cells will be generated. The PI will use approaches of integrative physiology and cell biology to find answers for the questions raised.