Insomnia and obstructive sleep apnoea (OSA) are more prevalent in patients with type 2 diabetes than in the general population. The association between OSA and metabolic abnormalities such as insulin resistance and type 2 diabetes has been generally characterized using several lines of parallel inquiry.
Studies that have used polysomnography to characterize breathing abnormalities during sleep have by and large found an independent association between OSA and metabolic dysfunction. OSA severity, as assessed by the AHI and severity of nocturnal oxyhemoglobin desaturation, has been associated with a repertoire of metabolic parameters including higher fasting insulin and glucose levels, a high prevalence of an abnormal oral glucose tolerance test, and impaired insulin sensitivity as assessed by hyperinsulinemic euglycemic clamp. Moreover, consideration for confounding factors such as age, BMI, and waist circumference in many of the published studies has provided credence to the hypothesis that OSA is independently, and perhaps causally, associated with metabolic abnormalities including type II diabetes.
Several animal and human studies have shown that intermittent hypoxia and sleep fragmentation can initiate a repertoire of pathophysiological effects that can alter normal glucose homeostasis. Exposure to conditions of sustained or intermittent hypoxia can decrease in insulin sensitivity and impair insulin secretion, defects that are fundamental to the pathogenesis of type 2 diabetes. Thus, OSA is likely to be of relevance in the older adult who is likely to have a higher predisposition for OSA and for metabolic dysfunction. Furthermore, OSA related disruption of sleep continuity may also adversely affect glucose metabolism.
The mechanisms through which intermittent hypoxemia and sleep fragmentation could affect glucose metabolism are summarized in Fig. 1:
- Alterations in sympathetic nervous system activity
- Changes in activity of hypothalamic-pituitary-adrenal (HPA) axis
- Formation of reactive oxygen species
- Increases in inflammatory cytokines (ie, interleukin-6) and tumor necrosis factor-α and adipocyte derived factors (ie, leptin, adiponectin, and resistin).
References
- Moon, K., Punjabi, N. M., & Aurora, R. N. (2015). Obstructive Sleep Apnea and Type 2 Diabetes in Older Adults. Clinics in Geriatric Medicine, 31(1), 139–ix. http://doi.org/10.1016/j.cger.2014.08.023
