objectives Obstructive sleep apnoea syndrome (OSAS) is strongly associated with obesity and characterized by endocrine and metabolic changes including impairment of insulin sensitivity. The aim of this study was to further clarify the insulin dynamics and glucose metabolism in this condition.
design, patients and measurements We studied 30 obese patients with OSAS [OSA, 21 males, 9 females; age, mean ± SEM: 53·1 ± 1·7 years; body mass index (BMI): 38·6 ± 1·1 kg/m2; waist-to-hip ratio (WHR): 0·99 ± 0·07; Apnoea/Hypopnoea Index (AHI): 40·5 ± 5·8 events/h of sleep] by means of overnight polysomnography and oral glucose tolerance testing. Mathematical models were used to assess: (i) whole-body insulin sensitivity index (ISI composite); (ii) hepatic ISI; (iii) the first phase of insulin secretion (ΔI30′−0′/ΔG30′−0′). Results were compared with those in 27 weight-matched patients with simple obesity (OB, 12 males, 15 females; age: 48·1 ± 2·8 years, BMI: 38·5 ± 1·4 kg/m2, WHR: 0·94 ± 0·09; AHI: 2·15 ± 0·5 events/h of sleep) and with 20 normal subjects (NS, 15 females; 5 males, age: 40·4 ± 2·9 years; BMI: 22·2 ± 0·6 kg/m2).
results ISI composite value was significantly lower in OSAS (1·71 ± 1·41) than in OB (3·08 ± 0·27) and in NS (6·1 ± 0·4) even after age-, BMI- and WHR-adjustment. Similarly, hepatic ISI was significantly different among the three groups (OB = 0·25 ± 0·02, OSAS = 0·16 ± 0·014 and NS = 0·55 ± 0·04). Sex did not affect ISI indices. Insulin secretion estimates were not significantly different among the three groups.
discussion Obese patients with obstructive sleep apnoea syndrome are more insulin resistant than patients with simple obesity independently of the degree and distribution of adiposity. The worsening in insulin sensitivity in obstructive sleep apnoea syndrome patients could reflect the hypoxic state and would account for the increased vascular risk in this condition.