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Regulation of Body Weight by Proopiomelanocortin Peptides in Humans: Lessons from the Nelson Syndrome
- Rajagopal V. Sekhar, MD;
- J. Clay Goodman, MD;
- Ashok Balasubramanyam, MD;
- Jeffrey B. Tatro, PhD; and
- Emese Mihaly, PhD
- From Baylor College of Medicine, Houston, TX 77030; Tufts University School of Medicine, Boston, MA 02111; and Semmelwies University Medical School, 1088 Budapest, Hungary.
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TO THE EDITOR:
Background: Melanocortins (α-melanocyte-stimulating hormone [MSH] and adrenocorticotropic hormone [ACTH]), in addition to their melanocyte-stimulating actions, may regulate energy balance through hypothalamic melanocortin-4 receptors (MC4Rs). In mice, deletion of the proopiomelanocortin (POMC) or MC4R genes leads to obesity, whereas administration of MC4R agonists (for example, MSH) causes weight loss (1). In humans, inactivating mutations of the POMC (2) or MC4R (3) genes can cause obesity, but there is no evidence that increased melanocortin action can cause weight loss.
In the Nelson syndrome, rapid growth of an adrenocorticotrophic pituitary adenoma following bilateral adrenalectomy causes extreme elevation of melanocortin levels and hyperpigmentation. The Nelson syndrome is a human model in which temporal associations among body weight, skin pigmentation, and …
