A β3-Adrenergic-Leptin-Melanocortin Circuit Regulates Behavioral and Metabolic Changes Induced by Chronic Stress

摘要: Background Obesity has been associated with an increased risk of developing several psychiatric illnesses, including major depression and posttraumatic stress disorder. Likewise, these stress-related disturbances are a higher rate obesity; yet, the neurobiological mechanisms linking obesity remain incompletely understood. Methods Following exposure to chronic social defeat (CSDS), mice were given free access either regular chow or Western-style diet high in triglycerides cholesterol. Comprehensive metabolic behavioral testing was then conducted. Results Mice subjected CSDS fed high-fat for 30 days display severe deficits accompanied by redistribution body fat. Stressed have decreased adipose tissue as well serum leptin levels compared control mice. Pharmacological inhibition β 3 -adrenergic signaling during normalizes abnormalities but worsens symptoms. Furthermore, central resistance reduced expression pro-opiomelanocortin hypothalamus. Administration melanocortin agonist stress-induced deficits, while lacking melanocortin-4 receptor attenuated Conclusions These results indicate that through receptors is adaptive response improves function. However, responses come at expense alterations contribute significant long-lasting abnormalities.