Sleep deprivation caused a 30% decline in the insulin sensitivity of fat cells of healthy, lean young adults, according to a study in the Oct. 6 issue of Annals of Internal Medicine.
Restricting sleep for 4 nights markedly impaired the phosphorylation of Akt within the adipocytes in subcutaneous fat, which is a crucial early step in the pathway that mediates most of insulin's metabolic action. "This finding identifies for the first time a molecular mechanism that may be involved in the reduction in total-body insulin sensitivity consistently observed in multiple laboratory studies of partial sleep deprivation in healthy adults," said Josiane L. Broussard, Ph.D., and her associates at the University of Chicago.
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A recent study says that sleep deprivation caused a 30% decline in the insulin sensitivity of fat cells and a 16% decline in total-body insulin sensitivity.
Moreover, "our finding of marked alterations in adipocyte function after experimental sleep restriction challenges the widely held belief that the primary function of sleep is the restoration of central nervous system function and suggests that sleep may play an equally important role in peripheral energy metabolism," they noted.
Insufficient sleep is known to raise the risk of metabolic disturbances, particularly insulin resistance, obesity, and type 2 diabetes. But "to our knowledge, no studies to date have linked sleep restriction to alterations in molecular metabolic pathways in any peripheral human tissue." Dr. Broussard and her colleagues examined whether experimental sleep restriction would reduce insulin sensitivity in subcutaneous fat, "a peripheral tissue that is a key site of insulin action and plays a pivotal role in energy metabolism as well as in the communication of energy balance to the brain."
Six men and one woman aged 18-30 years (mean age 23.7 years) who were healthy and lean were selected from the community as study subjects. All reported routine sleep times of 7.5-8.5 hours/night. All underwent overnight polysomnography to ensure they had no sleep disorders, standard glucose tolerance testing to rule out any occult disorders of insulin metabolism, and standard laboratory tests to rule out any other problem that could affect either sleep or metabolism.
These subjects were then assessed under two experimental sleep conditions in randomized order: after 4 consecutive nights of 8.5 hours of normal sleep and after 4 consecutive nights of 4.5 hours of restricted sleep. The subjects lived as sedentary inpatients during these experiments, with strictly controlled diets that were identical under the two sleep conditions.
At the conclusion of the sleep periods, abdominal subcutaneous fat tissue was sampled for in vitro measurement of phosphorylated Akt in response to increasing doses of insulin. Total body insulin sensitivity also was assessed using frequently sampled intravenous glucose tolerance tests.
The study subjects averaged 8.78 hours of sleep per night under the normal sleep condition and 4.35 hours under the restricted sleep condition. The amount of REM sleep was reduced by 56.8% in the latter condition.
After normal sleep, insulin provocation caused dose-dependent increases in phosphorylated Akt, as expected. In dramatic contrast, sleep restriction consistently induced an approximately 30% reduction in phosphorylated Akt in response to insulin provocation.
In addition, total-body insulin sensitivity was reduced by 16% after partial sleep deprivation, compared with normal sleep.
The 30% decline "lies within the range of the difference in insulin sensitivity in adipocytes from obese vs. lean participants and from diabetic patients vs. nondiabetic participants" in previous studies. "Thus, the impairment of insulin signalling in adipocytes from persons who are chronically sleep-deprived or have sleep disorders is likely to have important metabolic consequences," Dr. Broussard and her associates wrote (Ann. Intern. Med. 2012;157:549-57).
"From a clinical standpoint, our study provides additional evidence that insufficient sleep may contribute to the development of or exacerbate metabolic disorders." But the findings also "shed novel light on the still-elusive function of sleep, traditionally conceptualized as necessary only for the brain, because they suggest that sleep plays an important role for the functional integrity of multiple peripheral cell types, as well as for whole-body energy homeostasis," they said.
This study was limited in that it was performed at a single center, involved a very small sample size and involved only one woman. "The findings will therefore need to be replicated in a larger and more diverse population," the researchers added.
This study was funded by the National Institutes of Health. The researchers reported having no relevant conflicts of interest.