Melanin concentrating hormone: a functional melanocortin antagonist
in the hypothalamus.
Ludwig, David S., Kathleen G. Mountjoy, Jeffrey B. Tatro, Jennifer A.
Gillette, Robert C. Frederich Jeffrey S. Flier, and Eleftheria
Maratos-Flier.
Division of Endocrinology and Metabolism Division of Endocrinology,
Department of Medicine Department of Medicine, Beth Israel-Deaconess
Medical Center University of Kentucky, Boston, MA 02215 Chandler
Medical Center, Lexington, KY 40536. Division of Endocrinology
Division of Endocrinology, Department of Medicine Metabolism and
Molecular Medicine, Children's Hospital Department of Medicine and
Boston, MA 02115 Tupper Research Institute, Tufts University School
of Medicine, New England Medical Center, Boston, MA 02111. Research
Center for Developmental Elliott P. Joslin Research Laboratory,
Medicine and Biology Joslin Diabetes Center, University of Auckland
One Joslin Place, Private Bag 92019 Boston, MA 02215, Auckland, New
Zealand
APStracts 4:0285E, 1997.
Melanin concentrating hormone (MCH) and alpha-melanocyte stimulating
hormone (_"_MSH) demonstrate opposite actions on skin coloration
in teleost fish. Both peptides are present in the mammalian brain,
although their specific physiologic roles remain largely unknown. In
this study, we examined the interactions between MCH and _"_MSH
after intracerebroventricular administration in rats. MCH increased
food intake in a dose-dependent manner and lowered plasma
glucocorticoid levels through a mechanism involving
adrenocorticotropic hormone. In contrast, _"_MSH decreased food
intake and increased glucocorticoid levels. MCH, at a two-fold molar
excess, antagonized both actions of _"_MSH. _"_MSH, at a
three-fold molar excess, blocked the orexigenic properties of MCH.
MCH did not block _"_MSH binding or the ability of _"_MSH to
induce cAMP in cells expressing either the MC3 or MC4 receptor, the
principal brain _"_MSH receptor subtypes. These data suggest that
MCH and _"_MSH exert opposing and antagonistic influences on
feeding behavior and the stress response, and may function in a
coordinate manner to regulate metabolism through a novel mechanism
mediated in part by an MCH receptor.
Received 20 June 1997; accepted in final form 16 December 1997.
APS Manuscript Number E292-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 7 January 1998