Nocturnal Hypoxemia Causes Hyperglycemia in Patients With Obstructive Sleep Apnea and Type 2 Diabetes Mellitus

Background: Our purpose was to investigate the relationship between oxygen saturation (SpO(2)) and dynamic interstitial glucose level (IGL) in patients with obstructive sleep apnea (OSA) along with type 2 diabetes mellitus (T2DM), and to investigate the potential mechanisms thereof. Materials and Methods: A total of 130 patients with OSA and T2DM underwent polysomnography and oral glucose tolerance tests at the Sleep Medicine Center. Using the lowest (L) SpO(2)% tested, patients were divided into mild, moderate and severe LSpO(2) groups. Polysomnography and continuous glucose monitoring systems were used to analyze the altered pattern of SpO(2) and dynamic IGL in the 3 groups. Results: LSpO(2) during sleep in patients with OSA and T2DM stimulated an increase in IGL. The moderate and severe levels were represented by IGL 45 and IGL 30, respectively. The average nocturnal and peak IGL after LSpO(2) in the severe group were significantly higher than in the mild and moderate groups. Stepwise multiple regression analysis showedt hat the body mass index (beta = 0.301, P < 0.001), homeostatic model assessment of insulin resistance (beta = 0.260, P < 0.001), apnea-hypopnea index (beta = 0.309, P < 0.001), average SpO(2) (beta = -0.423, P = 0.008), LSpO(2) (beta = -0.369, P < 0.001) and microarousal index (beta = 0.335, P = 0.044) were probably related to nocturnal IGL in patients with OSA along with T2DM. Conclusions: Severe and moderate OSA with T2DM is marked by a delayed IGL peak following LSpO(2). Nocturnal hypoxemia causes hyperglycemia in patients with OSA along with T2DM.