Obesity in the mouse model of pro-opiomelanocortin deficiency responds to peripheral melanocortin

Linda Yaswen, Nicole Diehl, Miles B. Brennan, Ute Hochgeschwender

Research output: Contribution to journalArticlepeer-review

819 Scopus citations

Abstract

Pro-opiomelanocortin (POMC)-derived peptides (the melanocortins adrenocorticotropin, α-, β- and γ-melanocyte stimulating hormone; and the endogenous opioid β-endorphin) have a diverse array of biological activities, including roles in pigmentation, adrenocortical function and regulation of energy stores, and in the immune system and the central and peripheral nervous systems. We show here that mice lacking the POMCderived peptides have obesity, defective adrenal development and altered pigmentation. This phenotype is similar to that of the recently identified human POMC-deficient patients. When treated with a stable α-melanocyte- stimulating hormone agonist, mutant mice lost more than 40% of their excess weight after 2 weeks. Our results identify the POMC-null mutant mouse as a model for studying the human POMC-null syndrome, and indicate the therapeutic use of peripheral melanocortin in the treatment of obesity.

Original languageEnglish
Pages (from-to)1066-1070
Number of pages5
JournalNature Medicine
Volume5
Issue number9
DOIs
StatePublished - Sep 1999

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