Obstructive Sleep Apnea, Circadian Clock Disruption, and Metabolic Consequences

Overview

Journal Metabolites

Publisher MDPI

Date 2023 Jan 21

PMID 36676985

Authors

Mikolaj Malicki

Filip Franciszek Karuga

Bartosz Szmyd

Marcin Sochal

Agata Gabryelska

Affiliations

Soon will be listed here.

Abstract

Obstructive sleep apnea (OSA) is a chronic disorder characterized by recurrent episodes of apnea and hypopnea during sleep. It is associated with various cardiovascular and metabolic complications, including type 2 diabetes mellitus (T2DM) and obesity. Many pathways can be responsible for T2DM development in OSA patients, e.g., those related to HIF-1 and SIRT1 expression. Moreover, epigenetic mechanisms, such as or , are postulated to play a pivotal role in this link. It has been proven that OSA increases the occurrence of circadian clock disruption, which is also a risk factor for metabolic disease development. Circadian clock disruption impairs the metabolism of glucose, lipids, and the secretion of bile acids. Therefore, OSA-induced circadian clock disruption may be a potential, complex, underlying pathway involved in developing and exacerbating metabolic diseases among OSA patients. The current paper summarizes the available information pertaining to the relationship between OSA and circadian clock disruption in the context of potential mechanisms leading to metabolic disorders.

Citing Articles

Impact of Sleep Fragmentation and Arousal on Nonalcoholic Fatty Liver Disease in Patients with Obstructive Sleep Apnea: A Cross-Sectional Study.

Zhong Y, Wang B, Huang J, Nian M, Zhao J, Chen G Nat Sci Sleep. 2024; 16:2143-2150.

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Exploring the pharmacological mechanisms for alleviating OSA: Adenosine A2A receptor downregulation of the PI3K/Akt/HIF‑1 pathway (Review).

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Novel assessment of CPAP adherence data reveals distinct diurnal patterns.

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The Complex Relationship between Neuromodulators, Circadian Rhythms, and Insomnia in Patients with Obstructive Sleep Apnea.

Gabryelska A, Turkiewicz S, Ditmer M, Gajewski A, Strzelecki D, Bialasiewicz P Int J Mol Sci. 2024; 25(15).

PMID: 39126038 PMC: 11313237. DOI: 10.3390/ijms25158469.

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