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Melanin-concentrating hormone and food intake control: Sites of action, peptide interactions, and appetition.

Authors
  • Lord, Magen N1
  • Subramanian, Keshav2
  • Kanoski, Scott E3
  • Noble, Emily E4
  • 1 Department of Foods and Nutrition, University of Georgia, Athens, GA 30606, USA. , (Georgia)
  • 2 Neuroscience Graduate Program, University of Southern California, Los Angeles, CA 90089, USA.
  • 3 Neuroscience Graduate Program, University of Southern California, Los Angeles, CA 90089, USA; Human and Evolutionary Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089, USA. Electronic address: [email protected]
  • 4 Department of Foods and Nutrition, University of Georgia, Athens, GA 30606, USA. Electronic address: [email protected] , (Georgia)
Type
Published Article
Journal
Peptides
Publication Date
Dec 25, 2020
Volume
137
Pages
170476–170476
Identifiers
DOI: 10.1016/j.peptides.2020.170476
PMID: 33370567
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Given the increased prevalence of obesity and its associated comorbidities, understanding the mechanisms through which the brain regulates energy balance is of critical importance. The neuropeptide melanin-concentrating hormone (MCH) is produced in the lateral hypothalamic area and the adjacent incerto-hypothalamic area and promotes both food intake and energy conservation, overall contributing to body weight gain. Decades of research into this system has provided insight into the neural pathways and mechanisms (behavioral and neurobiological) through which MCH stimulates food intake. Recent technological advancements that allow for selective manipulation of MCH neuron activity have elucidated novel mechanisms of action for the hyperphagic effects of MCH, implicating neural "volume" transmission in the cerebrospinal fluid and sex-specific effects of MCH on food intake control as understudied areas for future investigation. Highlighted here are historical and recent findings that illuminate the neurobiological mechanisms through which MCH promotes food intake, including the identification of various specific neural signaling pathways and interactions with other peptide systems. We conclude with a framework that the hyperphagic effects of MCH signaling are predominantly mediated through enhancement of an "appetition" process in which early postoral prandial signals promote further caloric consumption. Copyright © 2020 Elsevier Inc. All rights reserved.

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