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This version published online on May 24, 2007
Endocrinology, doi:10.1210/en.2007-0017
A more recent version of this article appeared on September 1, 2007
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Submitted on January 11, 2007
Accepted on May 17, 2007

Regulation of central melanocortin signaling by interleukin-1{beta}

Jarrad M. Scarlett, Erin E. Jobst, Pablo J. Enriori, Darren D. Bowe, Ayesha K. Batra, Wilmon F. Grant, Michael A. Cowley, and Daniel L. Marks*

Center for the Study of Weight Regulation and Associated Disorders, Oregon Health and Science University, Portland, Oregon 97239; Department of Pediatrics, Oregon Health and Science University CDRCP, Portland, Oregon 97239; Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, Oregon 97006; School of Physical Therapy, Pacific University, Hillsboro, Oregon 97123

* To whom correspondence should be addressed. E-mail: marksd{at}ohsu.edu.

Anorexia and involuntary weight loss are common and debilitating complications of a number of chronic diseases and inflammatory states. Proinflammatory cytokines, including interleukin-1{beta} (IL-1{beta}), are hypothesized to mediate these responses through direct actions on the central nervous system. However, the neural circuits through which proinflammatory cytokines regulate food intake and energy balance remain to be characterized. Here we report that IL-1{beta} activates the central melanocortin system, a key neuronal circuit in the regulation of energy homeostasis. Proopiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARC) were found to express the type I interleukin-1 receptor. Intracerebroventricular injection of IL-1{beta} induced the expression of Fos protein in ARC POMC neurons, but not in POMC neurons in the commissural nucleus of the tractus solitarius (NTS). We further show that IL-1{beta} increases the frequency of action potentials of ARC POMC neurons and stimulates the release of {alpha}-melanocyte-stimulating hormone ({alpha}-MSH) from hypothalamic explants in a dose-dependent fashion. Collectively, our data support a model in which IL-1{beta} increases central melanocortin signaling by activating a subpopulation of hypothalamic POMC neurons and stimulating their release of {alpha}-MSH.
Key words: Proopiomelanocortin (POMC) • interleukin-1 beta (IL-1{beta}) • hypothalamus • nucleus of the tractus solitarius (NTS) • neuronal activation • energy homeostasis




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