Obesity and type II diabetes are 21st century pandemia. These metаbolic disorders are in the focus of attention of various specialties: cardiologists, endocrinologists, nutritionists, therapists, and others. The high incidence of obesity and type II diabetes cardiovascular complications, such as myocardial infarction, stroke, chronic heart failure, dementia, determine the call of risk factors search. Modifiable factors may include sleep disturbances. Recent studies have revealed a connection between changes in sleep duration and metabolic disorders. However, to date, the mechanisms underlying this association have not been established. The aim of the review is to summarize existing epidemiological and experimental observations, as well as an analysis of possible pathophysiological mechanisms linking sleep duration with obesity and type II diabetes. The article considers current data suggesting a bi-directional association of sleep disorders with obesity and diabetes. Sleep disturbances are significant determinant of developing metabolic disorders. Sleep duration correction as one of therapeutic targets for cardiovascular complications of obesity and type II diabetes prevention.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) is epidemiologically related to adverse cardiovascular outcomes. The pathophysiology clues are metabolic changes and obesity. The most studied anthropometric predictors of obesity, such as body mass index (BMI), waist circumference (WC), are influenced by various factors such as sex, type of constitution, hydration balance. The normal range of BMI and WC limits the diagnostic search for metabolic disturbances and visceral obesity in patients with respiratory sleep distress and can lead to increased cardiovascular risks. AIMS: to investigate the visceral obesity predictors in normal weight patients with obstructive sleep apnea syndrome. MATERIALS AND METHODS: We had performed а cross-sectional study, 68 patients were examined with mean age of 38.24 7.4 years. The main group (38 individuals) was represented by patients with OSAS. The control group consisted of healthy individuals without OSAS. Alternative markers of visceral obesity, such as lipid accumulation products, visceral obesity index, conicity index have been studied. RESULTS: In the main group we found different disorders of lipid metabolism such as the increase in triglyceride levels by 94%, low-density lipids by 32%, total cholesterol by 10% compared with the control group. Anthropometric evidence was obtained for excessive fat accumulation in patients with normal body weight and OSAS: WC was 89.6 5.7 cm in the main group and was higher than in the control group 83.7 6.3 cm (p = 0.024) due to an increase in the visceral fat compartment, as evidenced by the conicity index (67.2 7.0 and 59.3 6.2 respectively, p = 0.032) and waist to height ratio (0.58 0.05 and 0.53 0.04 in the main and control groups, respectively, p = 0.041). Correlation relationships between the severity of sleep apnea syndrome and visceral obesity indicators were revealed. CONCLUSIONS: Normal weight patients with breathing disorders are at risk of visceral fat obesity and, thereby, increased cardiovascular risk. Assessment of additional markers of visceral obesity in patients with normal body weight and sleep apnea is recommended to include in the dynamic observation programms.

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