Sleep disorders and the development of insulin resistance and obesity

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Journal: Endocrinology and Metabolism Clinics of North America

Publication Date: 09/2014

Summary: Sleep, which comprises a third of the human lifespan, consists of two major states, non-rapid eye movement (NREM, stages N1–3) and rapid eye movement (REM). Sleep is a physiologic state of decreased metabolism and likely serves a reparative role, marked by increased glycogen stores and peptide synthesis. Normal sleep is characterized by reduced glucose turnover by the brain and other metabolically active tissues, particularly during NREM sleep. Circadian and sleep-related changes in glucose tolerance occur in normal subjects, but there are conflicting data regarding lipid metabolism during sleep. Sleep duration has decreased over the last several decades, and with this have come cross-sectional and longitudinal data suggesting a link between short sleep duration and the prevalence of type 2 diabetes. Forced decreased sleep duration in healthy individuals has also been linked to impaired glucose homeostasis. Moreover, short sleep duration has been suggested to lead to obesity, although this is less conclusive since psychological and social factors also considerably impact food intake. Obstructive sleep apnea (OSA) is a disorder of sleep characterized by diminished or abrogated airflow, which results in intermittent hypoxia and sleep fragmentation. Based on a large body of evidence, this disorder seems to be associated with impaired glucose tolerance. Obesity is a major risk factor for the development of OSA, but whether OSA leads to obesity is unclear. Thus, the quality and quantity of sleep may have a profound effect on obesity and type 2 diabetes, and therefore should be routinely assessed in endocrine clinic.

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