To investigate the association between sleep disorder and osteoporosis in elderly female patients with type 2 diabetes.

Five hundred and thirty-six elderly female patients with type 2 diabetes aged above 60 years were recruited from July 2011 to July 2014. They were divided into two groups according to Pittsburgh Sleep Quality Index: patients without sleep disorder and patients with sleep disorder. The bone mineral density of femoral neck, Wards triangle, greater trochanter and lumbar spines(L2-L4) was measured by dual-energy X-ray absorptiometry. The groups were further divided into osteoporosis negative group and osteoporosis group. Biochemical indicators were detected in the two groups. Oral glucose tolerance test, insulin releasing test and glucagon releasing test were performed. We compared the differences of bone mineral density as well as α-cell and β-cell function after fasting and glucose-load. The Logistic regression analysis was performed to analyze sleep disorder as well as osteoporosis and other indicators.

(1)The bone mineral density of femoral neck, Wards triangle, greater trochanter and lumbar spines(L2-L4) was significantly lower(t=2.9652-6.3403, all P<0.05) and the prevalence of osteoporosis was significantly higher in patients with sleep disorder compared to those in patients without sleep disorder(χ²=13.891, P<0.05). Bone mineral density of sleep disorder subgroup was lower than those without sleep disorder, especially for greater trochanter and lumbar spines(L2-L3). (2) The level of glucagon at each time point and area under curve of glucagon as well as 0, 30, 180 min glucagon/insulin ratio and 0, 30, 60, 180 min glucagon/glucose ratio were significantly higher in patients with sleep disorder than those in patients without(t=1.0332-19.6437, all P<0.05). The levels of glycated hemoglobin A1c(HbA_1c), fructosamine, fasting insulin, homeostasis model assessment of insulin resistance index (HOMA-IR) were significantly higher in patients with sleep disorder compared to those without sleep disorder ((8.0%±1.9%) vs (7.3%±1.6%), (0.32±0.10) vs (0.30±0.08)mmol/L, (13±4) vs (12±4)mU/L, (4.7±0.8) vs(3.8±0.8), t=4.5956, 2.5445, 2.9871, 11.8356, all P<0.05). Insulin sensitivity index was lower in patients with sleep disorder than that in patients without sleep disorder (-4.2±0.5 vs -4.0±0.4, t=4.1559, P<0.05). Significant changes of the above indicators were observed in sleep disorder subgroup compared to those without sleep disorder(all P< 0.05). (3) Logistic regression analysis showed that sleep disorder was positively related to HOMA-IR, HbA_1c and area under curve of glucagon (OR=2.452, 1.119, 1.223, all P<0.05), whereas osteoporosis was positively related to postmenopausal duration, HbA_1c, area under curve of glucagon and sleep disorder(OR= 20.677, 19.948, 23.445, 23.682, all P<0.05).

Sleep disorder may be associated with osteoporosis via influencing islet α-cell and β-cell functions in elderly female patients with type 2 diabetes.

Diabetes mellitus, type 2; Sleep disorder; Osteoporosis; Islet α-cell; Islet β-cell