Interacting epidemics? Sleep curtailment, insulin resistance, and obesity

Ann N Y Acad Sci. 2012 Aug;1264(1):110-34. doi: 10.1111/j.1749-6632.2012.06655.x. Epub 2012 Jul 24.


In the last 50 years, the average self-reported sleep duration in the United States has decreased by 1.5-2 hours in parallel with an increasing prevalence of obesity and diabetes. Epidemiological studies and meta-analyses report a strong relationship between short or disturbed sleep, obesity, and abnormalities in glucose metabolism. This relationship is likely to be bidirectional and causal in nature, but many aspects remain to be elucidated. Sleep and the internal circadian clock influence a host of endocrine parameters. Sleep curtailment in humans alters multiple metabolic pathways, leading to more insulin resistance, possibly decreased energy expenditure, increased appetite, and immunological changes. On the other hand, psychological, endocrine, and anatomical abnormalities in individuals with obesity and/or diabetes can interfere with sleep duration and quality, thus creating a vicious cycle. In this review, we address mechanisms linking sleep with metabolism, highlight the need for studies conducted in real-life settings, and explore therapeutic interventions to improve sleep, with a potential beneficial effect on obesity and its comorbidities.

Publication types

  • Research Support, N.I.H., Intramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adiponectin / analysis
  • Appetite
  • Diabetes Mellitus / epidemiology*
  • Energy Metabolism*
  • Female
  • Ghrelin
  • Glucose / metabolism
  • Humans
  • Insulin Resistance*
  • Leptin
  • Male
  • Melatonin / metabolism
  • Obesity* / epidemiology
  • Obesity* / etiology
  • Obesity* / metabolism
  • Risk Factors
  • Sleep Deprivation / epidemiology*
  • Sleep Wake Disorders / epidemiology


  • Adiponectin
  • Ghrelin
  • Leptin
  • Glucose
  • Melatonin