Impact of Sleep and Circadian Disruption on Energy Balance and Diabetes: A Summary of Workshop Discussions

Abstract

A workshop was held at the National Institute for Diabetes and Digestive and Kidney Diseases with a focus on the impact of sleep and circadian disruption on energy balance and diabetes. The workshop identified a number of key principles for research in this area and a number of specific opportunities. Studies in this area would be facilitated by active collaboration between investigators in sleep/circadian research and investigators in metabolism/diabetes. There is a need to translate the elegant findings from basic research into improving the metabolic health of the American public. There is also a need for investigators studying the impact of sleep/circadian disruption in humans to move beyond measurements of insulin and glucose and conduct more in-depth phenotyping. There is also a need for the assessments of sleep and circadian rhythms as well as assessments for sleep-disordered breathing to be incorporated into all ongoing cohort studies related to diabetes risk. Studies in humans need to complement the elegant short-term laboratory-based human studies of simulated short sleep and shift work etc. with studies in subjects in the general population with these disorders. It is conceivable that chronic adaptations occur, and if so, the mechanisms by which they occur needs to be identified and understood. Particular areas of opportunity that are ready for translation are studies to address whether CPAP treatment of patients with pre-diabetes and obstructive sleep apnea (OSA) prevents or delays the onset of diabetes and whether temporal restricted feeding has the same impact on obesity rates in humans as it does in mice.

Keywords: circadian disruption; circadian rhythm; diabetes; insulin resistance; metabolism; obesity; short sleep; sleep apnea; sleep disorders.

© 2015 Associated Professional Sleep Societies, LLC.

Figures

Figure 1

Pathogenesis of obesity-related metabolic dysfunction. Studies of metabolic dysfunction in people need to provide a comprehensive approach and consider the complex changes that occur in multiple organs. Specifically, the following need to be assessed: (1) changes in adipose tissue biology that can be assessed by fat biopsies; (2) adipose tissue lipolytic activity and the release of free fatty acids (FFA) into the bloodstream; (3) adipokines; (4) metabolic changes in the liver, including intrahepatic triglyceride content; (5) very low density lipoprotein (VLDL) secretion rate; (6) de novo lipogenesis rates, fatty acid oxidation and liver insulin sensitivity; (7) changes in muscle insulin sensitivity and metabolite content, (8) β-cell function; (9) gut microbome; and (10) the brain plays an important role in glucose and lipid homeostasis, receiving information from periphery signals generated by food ingestion and subsequently contributing to the regulation of metabolism through innervation of metabolically active tissues such as muscle, pancreas, liver and adipose tissue. In obesity-related pathogenesis, increased sympathetic activation increases lipolysis and stimulates hepatic glucose production. Figure provided by Dr. Sam Klein.