| Objective: To reveal the interaction of sleep quality and sleep duration on glycemic control in patients with type 2 diabetes mellitus(T2DM). To analyze relevance of sleep quality with CVD in T2 DM patients and determine whether inflammation prompted by poor sleep has impact on the CVD. To investigate the relationship between poor sleep and diabetic kidney disease and to explore the roles of inflammatory markers in the pathogenetic process which poor sleep influence the morbidity of diabetic kidney disease.Methods: T2 DM patients hosipitalized in Tianjin Metabolic Diseases Hospital were enrolled in this study. Participants' sleep qualities were evaluated by Pittsburgh Sleep Quality Index(PSQI). “Good sleep quality” was defied as PQSI <5, “average sleep quality” was defied as PQSI 6–8, and “poor sleep quality” was defied as PQSI >8. The patients with PSQI score >5 were in the poor sleep group, and the others were in the good sleep group. Plasma samples of the patients were obtained to measure inflammatory markers and glycosylated hemoglobin(Hb A1c). Poor glycemic control was defied as Hb A1 c ?7%. Sleep duration was categorized as <6, 6–8, and >8 hours/night. Short sleep time was defied as sleep duration <6 hours/night.Results: 1. In the poor glycemic control group, the rate of patients who had insufficient sleep was much higher than that in the other group(?2=11.16, P=0.037). The rate of poor sleep quality in poor glycemic control group was much greater than that in the average control group(?2=9.79, P=0.007). After adjusted by gender, age, body mass index, and disease duration, the adjusted PSQI score's OR was 1.048(95% CI 1.007–1.092, P=0.023) for Hb A1 c level. The sleep duration's OR was 0.464(95% CI 0.236–0.912, P=0.026) for Hb A1 c level. One-way analysis of variance showed that the poor sleep quality group had the highest homeostasis model assessment-insulin resistance(P <0.01). 2. The morbidity of CVD was significantly higher in the poor sleep patients compared to the good sleep patients(P = 0.000). PSQI score ORs were both >1 for CVD in model 1 and model 2(P < 0.05). PSQI score were positively related to IL-6 and ICAM-1(P < 0.05), negatively to FBI(P < 0.05), but not related to CRP in linear regression models. Multiple logistic regression analysis showed IL-6 and ICAM-1, but not FBI and CRP, were related to CVD(P < 0.05). 3. The prevalence of diabetic kidney disease was higher in participants with poor sleep than with good sleep(41.8% vs. 24.8%,P=0.002). After adjustment, poor sleep(Pittsburg Sleep Quality Index score's OR 1.075 [95% CI 1.018-1.135],P=0.009) remained independently associated with diabetic kidney disease. Pittsburg Sleep Quality Index score were positively related to interleukin-6, intercellular adhesion molecule-1, P-selectin and fibroblast growth factor-23(P<0.05), but not related to fibrinogen and high sensitive C-reactive protein in linear regression models. Multiple logistic regression analysis showed that fibrinogen, intercellular adhesion molecule-1, P-selectin and fibroblast growth factor-23, but not interleukin-6 and high sensitive C-reactive protein, were risk factors of diabetic kidney disease.Conclusion: Inadequate sleep, in both quality and duration, should be regarded as a plausible risk factor for glycemic control in type 2 diabetes. Poor sleep is regarded as a plausible risk factor for CVD in T2 D patients, and may be mediated by certain inflammatory markers. Poor sleep is independently associated with diabetic kidney disease. Inflammatory markers may provide a pathogenic link between poor sleep and diabetic kidney disease. |
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