Subjective Sleep Complaints Are Associated With Insulin Resistance in Individuals Without Diabetes: The PPP-Botnia Study

• Autores: Antti-Jussi Pyykkönen, Bo Isomaa, Anu-Katriina Pesonen, Johan G. Eriksson, Leif Groop, Tllnamaija Tuomi, Katri Raikkonen
• Localización: Diabetes care, ISSN-e 0149-5992, Vol. 35, Nº. 11, 2012, págs. 2271-2278
• Idioma: inglés
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• Resumen

  • Sleep disorders and subjective sleep complaints have been associated with increased risk of type 2 diabetes. The evidence with respect to insulin resistance (IR) and insulin secretion in individuals without type 2 diabetes has been scarce and elusive. We examined if subjective sleep complaints and their co-occurrence were associated with IR and insulin secretion in adult women and men without diabetes. Women (n = 442) and men (n = 354) 18-75 years of age without type 2 diabetes underwent an oral glucose tolerance test (OGTT), with insulin and glucose measured at fasting and at 30 and 120 min. Complaints related to sleep apnea, insomnia, and daytime sleepiness were self-rated with the Basic Nordic Sleep Questionnaire. In comparison with individuals with no or minor sleep complaints, those with more frequent complaints of sleep apnea, insomnia, and daytime sleepiness were more insulin resistant, as evidenced by higher fasting insulin concentrations and insulin and glucose responses to OGTT, and more frequently had high homeostasis model assessment of IR and low insulin sensitivity index values. The likelihood of being insulin resistant increased significantly and linearly according to the accumulation of co-occurring sleep complaints. These associations changed only a little when adjusted for mediating and confounding factors and for depressive symptoms. Sleep complaints were not associated with indices of deficiency in insulin secretion. Subjective sleep complaints were associated with IR. The likelihood of being insulin resistant increased according to accumulation of co-occurring sleep complaints. Sleep complaints were not associated with deficiency in insulin secretion. [PUBLICATION ABSTRACT]