Insulin and obesity transform hypothalamic-pituitary-adrenal axis stemness and function in a hyperactive state

Metabolic diseases are an increasing problem in society with the brain-metabolic axis as a master regulator of human body for sustaining homeostasis under metabolic stress. However, inflammation and disease will trigger sustained activation hypothalamic-pituitary-adrenal axis. In this study, we investigated role stress on progenitor cells vitro, applied insulin leptin to murine isolated from pituitary adrenal cortex examined these hormones proliferation differentiation. vivo, two different mouse models disease, obesity leptin-deficient ob/ob mice achieved via feeding high-fat diet. Insulin was shown lead enhanced differentiation both adrenocortical progenitors. No alterations progenitors were noted our chronic models. hyperactivation observed expression appetite-regulating genes Npy Agrp changed hypothalamus adrenal. It is well-known that such glucocorticoids can induce changes including diabetes. article, show first time might be based early sensitization stem Thus, exposed high levels metabolically primed hyper-functional state leading hormone production. Likewise, obese animals exhibit hyperactive hyperplasia. This explain how life increase risk developing syndrome adulthood.