Over Time, Regular Sleep Deprivation May Lead to Metabolic Disorders Such as Diabetes and Obesity
Short-term sleep deprivation reduces insulin sensitivity in the body’s peripheral tissue, including fat cells. Over time, this can lead to metabolic disorders such as type 2 diabetes and obesity, as insulin helps to regulate appetite and energy metabolism. Results of this first-of-its-kind study are being published in the October 16 issue of Annals of Internal Medicine, the flagship journal of the American College of Physicians (ACP).
Seven healthy, lean men and women aged 18 to 30 were studied in a sleep lab during two study periods, at least four weeks apart. In random order, participants underwent four nights of 8.5 hours of sleep and four nights of 4.5 hours of sleep. Physical activity and caloric intake were strictly controlled regardless of sleep duration. At the end of each study period, researchers gave participants an intravenous glucose-tolerance test to measure total-body insulin sensitivity. The researchers also performed a biopsy of abdominal fat cells to measure how the fat cells responded to insulin. After four nights of restricted sleep, volunteers’ total-body insulin response decreased by an average of 16 percent, and insulin sensitivity of fat cells decreased by 30 percent. According to the researchers, this reduction is akin to taking the fat cell functioning of a healthy person down to that of an obese or diabetic patient.
“In our study, seven out of seven subjects had a significant change in insulin sensitivity after a brief period of sleep restriction,” said lead study author, Matthew Brady, PhD, Assistant Professor of Medicine and member of the Committee on Molecular Metabolism and Nutrition at the University of Chicago Medicine. “This is significant because sleeping four to five hours a night during the work week is not uncommon. People think they can function cognitively on little sleep, but our study proves they are not tolerating the metabolic consequences.”
According to the authors of an accompanying editorial, this is the first clinical study to examine the causal pathways by which reduced sleep duration may directly contribute to diabetes and obesity. They write that the study results point to a much wider influence of sleep on bodily functions, including metabolism, adipose tissue, cardiovascular function, and possibly more.
The editorial authors caution that the study did not specify whether researchers standardized participants’ exposure to light, so it is difficult to determine if changes in the functionality of adipocytes were due to sleep deprivation or duration of exposure to light (or darkness).
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