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Volume 58, Issue 1, Pages 16-21 (January 2009)


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Plasma α–melanocyte-stimulating hormone: sex differences and correlations with obesity

William T. Donahooa, Teri L. Hernandeza, Jessica L. Costabc, Dalan R. Jensena, Alison M. Morrisa, Miles B. Brennanb, Ute Hochgeschwenderd, Robert H. EckelaCorresponding Author Informationemail address

Received 15 October 2007; accepted 29 July 2008.

Abstract 

Rodent experiments raise the possibility of a regulatory role of peripheral α–melanocyte-stimulating hormone (α-MSH) in obesity and metabolism, but human data on peripheral α-MSH levels remain fragmentary. Because of the possible relationship between α-MSH and obesity, we endeavored to test the hypothesis that higher levels of α-MSH in obese patients would correlate with leptin levels and with other markers of obesity. Sixty normal-weight to obese healthy men and women participated. Weight, measures of body composition, and diet diaries were obtained; fasting blood was analyzed for α-MSH, lipids, glucose, insulin, leptin, and adiponectin. To begin to understand the source of peripherally measured hormones, α-MSH was also measured in serum samples from 5 individuals with untreated Addison disease. Levels of α-MSH were higher in men vs women (10.1 ± 4.3 vs 7.6 ± 3.4 pmol/L, P = .019), and α-MSH levels were higher in patients with Addison disease vs controls (17.7 ± 2.3 vs 8.7 ± 0.52 pmol/L, P < .001). Measures of adiposity correlated with insulin and leptin in men and women, and with adiponectin in women. α–Melanocyte-stimulating hormone levels did not correlate significantly with any parameter of adiposity or diet composition. The elevated α-MSH levels in patients with untreated Addison disease suggest possible pituitary secretion of α-MSH to the periphery. The lack of correlation between peripheral α-MSH and parameters of adiposity suggests that endogenous plasma α-MSH levels are not a metric for body composition per se.

a Division of Endocrinology, Metabolism, and Diabetes, University of Colorado Denver, P.O. Box 6511, Aurora, CO 80045, USA

b Department of Biology, Eleanor Roosevelt Institute, University of Denver, Denver, CO 80206, USA

c Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1142, New Zealand

d Developmental Biology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA

Corresponding Author InformationCorresponding author. Tel.: +1 303 724 3923.

PII: S0026-0495(08)00285-0

doi:10.1016/j.metabol.2008.07.028


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