Differential role of melanocortin receptor subtypes in cachexia.

摘要: Animals and humans respond to starvation with a complex neuroendocrine response that ultimately leads an increase in appetite, sparing of lean body mass (LBM) burning fat, overall decrease basal metabolic rate. In contrast, cachexia is pathological state malnutrition associated many infections chronic diseases, wherein appetite diminished concomitant rate, relative wasting LBM. previous studies, we demonstrated anorexia weight loss mouse models induced by lipopolysaccharide (LPS) administration tumor growth are ameliorated central melanocortin-4 (MC4) receptor (MC4-R) blockade. contrast the results seen MC4 blockade, melanocortin-3 (MC3) knockout (MC3-RKO) mice show illness-induced LPS cytokine administration, they have similar decreases mobility. Both MC3-RKOs MC4-RKOs intact corticosterone fever injection. models, MC4-RKO resist LBM brought about growth, whereas MC3-RKO animals enhanced tissue wasting. These data underscore importance melanocortin signaling homeostasis demonstrate differential effects MC3-R MC4-R blockade on development cachexia.