Obstructive Sleep Apnea Exacerbates Glucose Dysmetabolism and Pancreatic β-Cell Dysfunction in Overweight and Obese Nondiabetic Young Adults
Authors Li N, Fan Y, Zhou JP, Maimba OD, Zhang L, Li QY
Received 19 February 2020
Accepted for publication 5 June 2020
Published 10 July 2020 Volume 2020:13 Pages 2465—2476
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Juei-Tang Cheng
Ning Li,1,2,* Yun Fan,1,2,* Jian Ping Zhou,1,2,* Ocholi Don Maimba,3 Liu Zhang,1,2 Qing Yun Li1,2
1Department of Respiratory and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, People’s Republic of China; 2Institute of Respiratory Disease, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, People’s Republic of China; 3Department of Clinical Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Qing Yun Li
Department of Respiratory and Critical Care Medicine, Ruijin Hospital,Shanghai Jiao Tong University School of Medicine, No. 197 Ruijin 2nd Road, Shanghai 200025, People’s Republic of China
, Email firstname.lastname@example.org
Purpose: This study aimed to investigate the effects of obstructive sleep apnea (OSA) on the pancreatic β-cells dysfunction and their implications in the glucose dysmetabolism of overweight and obese nondiabetic young adults.
Materials and Methods: The cross-sectional analysis included 422 subjects (261 males/161 females) with the mean age of 27.77 ± 7.51 years and average body mass index (BMI) of 34.84 ± 5.69 kg/m2. All subjects underwent polysomnography (PSG), oral glucose tolerance-insulin releasing test (OGTT-IRT) and serum glycosylated hemoglobin A1 (HbA1c) measurement. The glucose metabolism and pancreatic β-cell function in relation to measures of OSA were determined adjustment for important confounders such as age and sex.
Results: OSA subjects accounted for 54.91% in the normal glucose tolerance (NGT) group and 72.11% in the prediabetes (preDM) group (P =0.001). HbA1c was the highest in the preDM subjects with severe OSA. In the NGT subjects, the 1-h glucose level significantly elevated with the OSA severity, and the homeostasis model assessment-β (HOMA-β) was negatively related to nocturnal mean SpO2 (P < 0.05). In the preDM subjects, HOMA-β, early phase insulinogenic index (∆I30/∆G30), total area under the curve of insulin in 180 min (AUC-I180), and the oral disposition index (DIO) were the lowest in the severe OSA group. DIO was associated with higher oxygen desaturation index (ODI) and lower nocturnal mean SpO2, and AUC-I180 was negatively related to TS90 (P < 0.05).
Conclusion: Our study indicated higher prevalence of OSA in overweight and obese nondiabetic young adults, especially preDM subjects. The impaired glucose tolerance was observed early after glucose intake in the NGT subjects. OSA induces compensatory increase in the pancreatic β-cell function in the NGT subjects, while pancreatic β-cell dysfunction is present in the preDM subjects with severe OSA.
Keywords: obstructive sleep apnea, obesity, nondiabetes, glucose tolerance, pancreatic β-cell function
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