Obesity as a mediator linking sleep-disordered breathing to both impaired fasting glucose and type 2 diabetes.

Pubmed ID: 36107360

Journal: Sleep & breathing = Schlaf & Atmung

Publication Date: June 1, 2023

Affiliation: Department of Health Statistics, School of Public Health, Shanxi Medical University, No.56 Xinjian South Road, Taiyuan, 030001, China. tongwang@sxmu.edu.cn.

MeSH Terms: Humans, Cross-Sectional Studies, Obesity, Diabetes Mellitus, Type 2, Obesity, Abdominal, Fasting, Sleep Apnea, Obstructive, Sleep Apnea Syndromes, Glucose, Hypoxia

Authors: Chen S, Wang J, Wang J, Wang T, Zhao X, Gao Q, Guan H

Cite As: Chen S, Wang J, Wang J, Gao Q, Zhao X, Guan H, Wang T. Obesity as a mediator linking sleep-disordered breathing to both impaired fasting glucose and type 2 diabetes. Sleep Breath 2023 Jun;27(3):1067-1080. Epub 2022 Sep 15.

Studies:

Abstract

PURPOSE: To examine whether or not associations between sleep-disordered breathing (SDB) and impaired fasting glucose and type 2 diabetes are mediated by obesity. METHODS: We used cross-sectional data including participants from the Multi-Ethnic Study of Atherosclerosis (MESA). SDB, including obstructive sleep apnea (OSA), hypoxia and sleep fragmentation, was evaluated by polysomnography. Further, five obesity measures related to overall obesity and central obesity were assessed. Mediation analysis was conducted to explore the mediating effect of obesity on these relationships between SDB and impaired fasting glucose and type 2 diabetes. RESULTS: Among 1615 participants, OSA and hypoxia, including apnea hypopnea index (AHI) ≥ 15, percent of total sleep time (TST) with SaO<sub>2</sub> &lt; 90% (TST90), oxygen desaturation index (ODI), and lowest oxygen saturation (SaO<sub>2</sub>), were significantly associated with impaired fasting glucose and type 2 diabetes. In addition, mean SaO<sub>2</sub> was also associated with impaired fasting glucose. Mediation analysis showed that these relationships were significantly mediated by all five obesity measures, where central obesity had greater mediating effect than overall obesity. Proportion of mediation of obesity ranged from 21.5 to 62.5% for impaired fasting glucose and 25.85 to 71.6% for type 2 diabetes, with substantial differences found in the subgroup analysis by gender or race/ethnicity. The consistency of the mediating effect was demonstrated across multiple measures of SDB, obesity, and glucose metabolism. CONCLUSION: Obesity, especially central obesity, may play a critical role in the pathway where SDB, including OSA and hypoxia, increases the occurrence of impaired fasting glucose and type 2 diabetes. Weight management is important for patients with SDB to prevent type 2 diabetes.