Energy Expenditure during Sleep Is an Independent Marker of Insulin-Resistance—A Cross-Sectional Study of Overweight/Obese Subjects

Abstract

Normal sleep is characterized by increased glycogen stores and reduced glucose turnover by metabolically active tissues, thus it is a state of decreased metabolism. It has been reported that reduced sleep quality is associated with increased insulin-resistance and disrupted metabolism. However, the relationship between energy expenditure during sleep (EEDS) and insulin-resistance (homeostasis model assessment, HOMA-IR) has not been clarified. The aim of this study was to investigate the role of EEDS in the association between sleep quality and insulin resistance. A total of 226 individuals [women 72.1%; mean (DS) age 50.46 (±13.1) years; BMI 33.4 (±8.41) Kg / m2] undergoing the oral glucose tolerance test (OGTT) were also asked to wear a metabolic holter (Armband) for 3-days, to assess their daily energy expenditure. The Armband is capable of measuring energy expenditure every minute, but also the duration and quality of sleep. The EEDS corrected for weight (EEDS/WEIGHT) was lower in patients with insulin resistance, HOMA-IR above 2.5 (p <.001). The EEDS/WEIGHT was inversely related to HOMA-IR (r = -0.23; p <.001) and directly to the quality of sleep (r = 0.15; p <.001). Using a multivariate linear regression, with sleep quality, age, gender, glucose and insulin area under the curve (AUC) and EEDS/ WEIGHT as independent variables, the HOMA-IR value was independently and significantly predicted by the insulin AUC (p <.001, beta = 0.538), by gender (p <.01, beta = 0.155) and by the EEDS/WEIGHT (p <.004, beta = -0.173). EEDS is an independent marker of insulin resistance. The mechanism underlying this correlation may be explained by the state of reduced glucose uptake during sleep, which it is further increased during insulin-resistance conditions, with a consequential reduction in energy production. This finding may provide another explanation to the inverse association between sleep quality and metabolic disorders such as type 2 diabetes and obesity. Disclosure D. Tuccinardi: None. E. Maddaloni: Speaker's Bureau; Self; Merck & Co., Inc.. Research Support; Self; European Foundation for the Study of Diabetes. I. Capasso: None. L. Rampa: None. A. Soare: None. D. Maggi: None. G. Defeudis: None. S. Kyanvash: None. A. Maurizi: None. P. Pozzilli: Research Support; Self; Sanofi. Speaker's Bureau; Self; Eli Lilly and Company. Research Support; Self; Merck Sharp & Dohme Corp.. S. Manfrini: None.