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Objective: To explore the association between retinopathy and sleep disorder in patients with type 2 diabetes mellitus (T2DM)., Methods: A total of 440 patients with T2DM treated from July 2011 to July 2013 in Metabolic Disease Hospital of Tianjin Medical University were divided into 2 groups according to Pittsburgh Sleep Quality Index: non-sleep disorder group (258 cases) and sleep disorder group (182 cases). Biochemical parameters including hepatorenal function, blood lipids, glycosylated hemoglobin (HbA1c), fructosamine and hemorrheology were detected. Oral glucose tolerance test, insulin releasing test and glucagon releasing test were performed to detect the inteR-group differences of α-cell and β-cell function after fasting and glucose-load management. The logistic regression analysis was performed to identify the factors relevant to retinopathy., Results: The ratio of retinopathy was 42.9% in sleep disorder group, which was higher compared to those in non-sleep disorder group (32.6%), P=0.027. The levels of fasting plasma glucose, postprandial blood glucose, HbA1c, fructosamine, systolic blood pressure, diastolic blood pressure and the indicators of hemorrheology (plasma viscosity, erythrocyte aggregation index, erythrocyte rigidity index, fibrinogen) were significantly higher in patients with sleep disorder compared to those without sleep disorder, while the erythrocyte defomation index was significantly lower in sleep disorder group (all P<0.05). The levels of glucagon and glucagon/insulin ratio at each time point as well as area under curve of glucagon were significantly higher in sleep disorder group (all P<0.05). The levels of fasting insulin, homeostasis model assessment for insulin resistance index (HOMA-IR) and area under curve of insulin were significantly higher in patients with sleep disorder compared to those without sleep disorder, while insulin sensitivity index was lower in patients with sleep disorder (all P<0.05). Logistic regression analysis showed that retinopathy was positively related to HbA1c (OR: 1.744-3.249), fibrinogen (OR: 1.687-2.998), systolic blood pressure (OR: 1.152-2.013), HOMA-IR (OR: 1.006-1.389) and sleep disorder (OR: 1.144-2.426), and negatively related to insulin sensitivity index (OR: 0.107-0.784) (all P<0.05)., Conclusion: Sleep disorders may be associated with retinopathy through multiple mechanisms in patients with T2DM.

Objective: To explore the association between sleep disorder and osteoporosis in elderly female patients with type 2 diabetes mellitus (T2DM)., Methods: A total of 536 elderly female T2DM patients from July 2011 to July 2014 were divided into two groups of patients without sleep disorder and those with sleep disorder based upon the Pittsburgh Sleep Quality Index. The bone mineral density of femoral neck, Wards triangle, greater trochanter and lumbar spines (L2-L4) were measured by dual-energy X-ray absorptiometry. Biochemical indicators were detected in two groups. Oral glucose tolerance and insulin releasing tests were performed. We compared the differences of bone mineral density and β-cell function after fasting and glucose-load. The logistic regression analyses were performed between sleep disorder and osteoporosis and other indicators., Results: The levels of high sensitivity C-reactive protein (hs-CRP), HbA1c, cortisol (COR), adrenocorticotropic hormone (ACTH), fasting insulin (FINS) and homeostasis model assessment-estimated insulin resistance (HOMA-IR) were significantly higher in patients with sleep disorder compared to those without sleep disorder [(3.5 ± 1.1) vs (2.6 ± 0.9) mg/L, (8.0 ± 1.9)% vs (7.3 ± 1.6)%, (512 ± 88) vs (436 ± 76) nmol/L, (6.4 ± 2.3) vs (5.1 ± 2.0) pmol/L, (13.4 ± 4.3) vs (12.4 ± 4.0) mU/L, 4.7 ± 0.8 vs 3.8 ± 0.8, all P < 0.05]. Insulin sensitivity index (ISI) was lower in patients with sleep disorder than that in patients without sleep disorder (-4.2 ± 0.5 vs -4.0 ± 0.4, P < 0.05). The bone mineral density of femoral neck, Wards triangle, greater trochanter and lumbar spines (L2-L4) were significantly lower and the prevalence rate of osteoporosis was significantly higher in patients with sleep disorder compared to those in patients without sleep disorder (all P < 0.05). Logistic regression analysis showed that sleep disorder was positively correlated with HOMA-IR, HbA1c, COR and ACTH (all P < 0.05) and negatively with ISI (P < 0.05). Logistic regression analysis showed that osteoporosis was positively correlated with postmenopausal duration, HbA1c, COR, ACTH and sleep disorder (all P < 0.05) and negatively with ISI (P < 0.05)., Conclusion: Sleep disorder causes osteoporosis through various mechanisms in elderly female T2DM patients. Improving sleep disorder may help to reduce the prevalence of osteoporosis.

Objective: To explore the association between sleep disorders and dawn phenomenon in patients with type 2 diabetes mellitus (T2DM)., Methods: From July 2011 to July 2014 at Metabolic Disease Hospital, Tianjin Medical University, 316 T2DM patients on continuous glucose monitoring were divided into two groups according to the Pittsburgh Sleep Quality Index, i.e. those without sleep disorders (n = 186) and those with sleep disorders (n = 130). Biochemical parameters including hepatorenal functions, blood lipids, glycosylated hemoglobin (HbA1c) and fructosamine were detected. Oral glucose tolerance test, insulin releasing test and glucagon releasing test were performed to detect the inter-group differences of glucose concentration and α-cell and β-cell functions after fasting and glucose loading. And the correlation and regression analyses were performed between sleep disorders and other parameters., Results: The level of HbA1c, fructosamine, increment of fasting glucose and nocturnal nadir glucose, glucose increment before and after breakfast, 24 h mean glucose, fasting insulin, homeostasis model assessment of insulin resistance index (HOMA-IR) and area under curve of insulin were significantly higher in patients with sleep disorders than those without sleep disorders (8.2% ± 2.0% vs 7.4% ± 1.7%, (0.33 ± 0.10) vs (0.29 ± 0.07) mmol/L, (1.511 ± 0.294) vs (0.889 ± 0.233) mmol/L, (2.144 ± 0.400) vs (1.522 ± 0.378) mmol/L, (9.917 ± 1.800) vs (8.694 ± 1.622) mmol/L, (13.49 ± 4.68) vs (12.16 ± 4.56) mU/L, 4.98 ± 0.90 vs 3.82 ± 0.82, (8.47 ± 0.59) vs (8.25 ± 0.54), all P < 0.05). Insulin sensitivity index was lower in patients with sleep disorders than that in those without sleep disorders (-4.28 ± 0.62 vs -4.03 ± 0.52, P < 0.05). The level of glucagon at each timepoint and area-under-curve of glucagon were significantly higher in patients with sleep disorders than those without sleep disorders. The levels of 0, 30, 180 min glucagon/insulin ratio and glucagon/glucose ratio were significantly higher in patients with sleep disorders (all P < 0.05). Sleep disorder was positively correlated with HOMA-IR, glucagon/insulin ratio, increment of fasting glucose and nocturnal nadir glucose and dawn phenomenon (all P < 0.05). Yet there was a negative correlation with insulin sensitivity index (P < 0.05)., Conclusions: Sleep disorders are associated with dawn phenomenon. And improving sleep disorder helps to improve the dawn phenomenon and optimize overall glycemic control.