Xap5 protects against necrotic apoptosis induced by overdevelopment in adipocytes.

The development and death of adipocytes play a crucial role in the metabolic stability of the body. We report that Xap5 plays a significant role in the development and death of adipocytes. The specific knockout of Xap5 in mature adipocytes leads to severe lipodystrophy in mice, subsequently causing metabolic disorders. By analyzing the development process of wild-type and Xap5 knockout adipocytes in vivo and in vitro, we found that the adipose deficiency caused by Xap5 knockout is mainly due to necroptosis caused by excessive development of adipocytes. Our results reveal a previously unrecognized role of Xap5 in adipocyte development and homeostasis. Overall design: To understand the physiological significance and function of Xap5 in regulating adipocyte development and cell death, we generated mature adipocyte-specific Xap5 knockout (KO) mice (Adiponectin-cKO mice). We then conducted gene expression profiling analysis using data from RNA-seq from white adipose tissue (WAT) of Xap5 wild-type (WT) and Adiponectin-cKO mice at postnatal day 42 (P42), and in-vitro cultured adipocytes of Xap5 WT and cKO mice after 8 days of adipogenic induction.