Obstructive Sleep Apnea Exacerbates Glucose Dysmetabolism and Pancreatic β-Cell Dysfunction in Overweight and Obese Nondiabetic Young Adults.

Abstract

PurposeThis 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 MethodsThe 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.ResultsOSA 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).ConclusionOur 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.