An Update on Obstructive Sleep Apnea and the Metabolic Syndrome

Jamie Lam; Mary Ip

Disclosures

Curr Opin Pulm Med. 2007;13(6):484-489. 

In This Article

Obstructive Sleep Apnea and Insulin Resistance/Glucose Intolerance/Diabetes Mellitus

Insulin resistance and visceral obesity are considered to be at the core of the constellation of risk factors that define the metabolic syndrome.[11] Insulin resistance is strongly associated with visceral obesity. OSA exhibits pathophysiologic mechanisms that may potentially contribute to the development of insulin resistance, including autonomic activation, alterations in neuroendocrine function, direct effects of hypoxemia on glucose regulation, and release of proinflammatory cytokines such as interleukin-6 and tumor necrosis factor-?.[29**,39,40]

A number of studies have looked at the association between OSA and insulin resistance/glucose intolerance.[29**,39] Epidemiologic data from the Sleep Heart Health Study[41] suggested that patients with mild or moderate to severe OSA have increased risks for fasting glucose intolerance after adjustment for confounding factors. Previous clinical studies including smaller samples of patients have yielded conflicting results, whereas recent studies have more consistently demonstrated an independent association between OSA and insulin resistance in adults,[29**,39,40,41,42] although this is by no means a universal finding.[43] In pediatric age groups, the results have also been conflicting.[10*,34*]

Insulin resistance is the hallmark of type II diabetes. A study of 1682 diabetic men in the UK[44*] estimated OSA prevalence at 23%, and OSA was significantly associated with diabetes, independent of age, BMI, and neck size. The Wisconsin Cohort Study[45] reported that 3% of individuals with an AHI below 5 had a diagnosis of type II diabetes, whereas 15% of those with an AHI of 15 or greater had diabetes, at a twofold relative risk after adjustment for age, sex, and body habitus. A 4-year follow up, however, did not confirm an increased incidence of diabetes after controlling for confounding factors, and thus a causal role for SDB in the development of diabetes cannot be established.

Interventional data on OSA and insulin resistance have mostly been observational, involving small samples of individuals. The effect of CPAP treatment on insulin resistance in nondiabetic OSA patients has been conflicting, and most studies failed to demonstrate any significant effect,[40] whereas one study showed improvement mainly in nonobese individuals.[46] Recently, a randomized controlled cross-over study of obese OSA men[19*] did not demonstrate any effect of CPAP treatment for 6 weeks on insulin resistance. Observational studies in OSA patients with diabetes[47,48] suggested that CPAP treatment may result in better glycemic control. These findings must be corroborated by randomized controlled trials before any conclusions can be drawn.

The effect of OSA on glucose homeostasis has been investigated in animal experiments. Exposure to chronic intermittent hypoxia led to an increase in insulin resistance in leptin-deficient obese mice.[49] Sympathetic activation is a putative mechanism in the development of insulin resistance in OSA, but a study of acute intermittent hypoxia in lean mice showed that insulin resistance occurred independent of autonomic activation.[50]

In summary, although there is growing evidence for an independent contribution of OSA to insulin resistance, the picture is far from complete.

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