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Leptin-mediated neural targets in obesity hypoventilation syndrome.

Abstract
Obesity hypoventilation syndrome (OHS) is defined as daytime hypercapnia in obese individuals in the absence of other underlying causes. In the United States, OHS is present in 10%-20% of obese patients with obstructive sleep apnea and is linked to hypoventilation during sleep. OHS leads to high cardiorespiratory morbidity and mortality, and there is no effective pharmacotherapy. The depressed hypercapnic ventilatory response plays a key role in OHS. The pathogenesis of OHS has been linked to resistance to an adipocyte-produced hormone, leptin, a major regulator of metabolism and control of breathing. Mechanisms by which leptin modulates the control of breathing are potential targets for novel therapeutic strategies in OHS. Recent advances shed light on the molecular pathways related to the central chemoreceptor function in health and disease. Leptin signaling in the nucleus of the solitary tract, retrotrapezoid nucleus, hypoglossal nucleus, and dorsomedial hypothalamus, and anatomical projections from these nuclei to the respiratory control centers, may contribute to OHS. In this review, we describe current views on leptin-mediated mechanisms that regulate breathing and CO2 homeostasis with a focus on potential therapeutics for the treatment of OHS.
AuthorsMateus R Amorim, O Aung, Babak Mokhlesi, Vsevolod Y Polotsky
JournalSleep (Sleep) Vol. 45 Issue 9 (09 08 2022) ISSN: 1550-9109 [Electronic] United States
PMID35778900 (Publication Type: Journal Article, Review, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Copyright© The Author(s) 2022. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For permissions, please e-mail: [email protected].
Chemical References
  • Leptin
Topics
  • Humans
  • Hypercapnia (complications)
  • Hypoventilation (complications)
  • Leptin (metabolism)
  • Obesity (complications)
  • Obesity Hypoventilation Syndrome (complications, therapy)

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