Abstract
Type 2 diabetes exerts a negative impact on sleep breathing. It is unknown whether a long-term improvement in glycemic control ameliorates this effect. We conducted an interventional study with 35 patients with type 2 diabetes and obstructive sleep apnea (OSA) to explore this. At home, sleep breathing parameters were assessed at baseline and after a 4-month period in which antidiabetic therapy was intensified. Patients who decreased their body mass index ≥2kg/m2 were excluded. Those with an HbA1c reduction ≥0.5% were considered good responders (n = 24). After the follow-up, good responders exhibited an improvement in the apnea–hypopnea index (AHI: 26-1 (95% IC: 8.6–95.0) vs. 20.0 (4.0–62.4) events/hour, p = 0.002) and in time with oxygen saturation below 90% (CT90: 13.3 (0.4–69.0) vs. 8.1 (0.4–71.2) %, p = 0.002). No changes were observed in the group of non–responders (p = 0.722 and p = 0.138, respectively). The percentage of moderate and severe OSA decreased among good responders (p = 0.040). In the wider population, the change in HbA1c correlated positively to decreases in AHI (r = 0.358, p = 0.035) and negatively to increases in the minimum arterial oxygen saturation (r = −0.386, p = 0.039). Stepwise multivariate regression analysis showed that baseline AHI and the absolute change in HbA1c independently predicted decreased AHI (R2 = 0.496). The improvement of glycemic control exerts beneficial effects on sleep breathing parameters in type 2 diabetes, which cannot be attributed merely to weight loss.
Highlights
In recent years, increasing evidence has appeared to support the idea that type 2 diabetes might contribute to the development of sleep breathing disorders characterized by sleep fragmentation and intermittent hypoxia [1]
In order to shed light on this issue, we present an interventional study aimed at examining whether the improvement of metabolic control during a three-month period in patients with type 2 diabetes leads to significant changes in sleep breathing parameters
No differences at baseline were observed between the groups regarding clinical, metabolic or nocturnal breathing parameters (Table S1)
Summary
In recent years, increasing evidence has appeared to support the idea that type 2 diabetes might contribute to the development of sleep breathing disorders characterized by sleep fragmentation and intermittent hypoxia [1]. Type 2 diabetes is an independent risk factor for excessive daytime sleepiness and almost two out of every three patients are categorized as “poor sleepers” [5]. This is a crucial finding because sleep-related hypoxemia and sleep fragmentation lead to sympathetic overactivity, endothelial dysfunction, an atherogenic lipid profile and increased blood pressure, factors that may contribute to the enhanced cardiovascular risk detected in type 2 diabetes [6,7]. The presence of some degree of diabetic autonomic neuropathy, with a powerlessness to respond appropriately to nocturnal airflow reductions, has been implicated in this relationship [8]
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