Mitochondria are involved in various cellular functions such as energy production and apoptosis, and their dysfunction has been regarded as one of the causes of metabolic disorders such as diabetes. We recently identified the mitochondrial protein p13 with a molecular weight of 13 kDa based on the decreased expression in pancreatic islets of Langerhans in type II diabetic mice, and have been conducting research using systemically deficient mice (p13-/- mice). Here, we investigated the role of p13 in white adipose tissue (WAT) pathophysiology via multiscale omics analyses in vivo and in vitro. First, we measured the weight of various tissues in the whole body and found that the weight of white adipose tissue was markedly decreased in p13-/- mice. Moreover, as a result of comprehensive histochemical analysis, selective and marked abnormalities were observed in p13-/- WAT compared to the other tissues, and especially, a marked reduction in the size of adipocytes and lipid droplets were observed. Besides, RNA-seq and qRT-PCR analyses revealed decreases in lipid synthesis genes and increases in lipid degradation genes in p13-/- WAT, suggesting the role of p13 in lipid metabolism. In contrast, there was no significant difference in adipose differentiation marker genes, and we also confirmed that p13 deficiency did not affect adipose differentiation in an adipocyte differentiation model using mouse embryonic fibroblasts (MEFs). Serum parameter analysis revealed high levels of total ketone bodies and low levels of blood glucose, lipase, triglycerides, and HDL-C. Besides, p13-/- mice had lower steady-state insulin levels and lower levels of insulin-antagonizing corticosterone. Taken together, the present results suggest that WAT is markedly decreased in p13-/- mice due to abnormal hormone homeostasis, and that endogenous p13 may play an important role in regulating hormon release and lipid metabolism.