Obtaining the proper duration and quality of sleep is important for the normal functioning of the human body and mind. Sleep is well known to be integral in the function of the central nervous system and influences memory formation and the learning process. Less intuitively, sleep has been found to impact several metabolic states. Epidemiological studies have shown that sleep deprivation can increase the risk of developing insulin resistance, type 2 diabetes, and obesity. We have previously discussed the finding that sleep deprivation increases the risk of developing insulin resistance and type 2 diabetes in teenagers. The exact mechanism whereby sleep influences peripheral metabolic conditions is not clearly understood, but these findings suggest that sleep plays an equally important role for both the central nervous system and peripheral metabolic functions.
Researchers, led by Dr. Matthew J. Brady from the University of Chicago, have found that sleep deprivation causes fat cells to have decreased responsiveness to insulin and to develop insulin resistance. The results of their study were published online in the journal Annals of Internal Medicine. The researchers conducted a randomized crossover study with seven healthy adults with an average age of 23 years and average BMI of 22. The study participants were studies while having 4.5 hours of sleep for four days and while having 8.5 hours of sleep for four days. Fat cells were collected from subcutaneous fat biopsy and their ability to respond to insulin was assessed by measuring levels of phosphorylated Akt . The phosphorylation of Akt is a crucial step in the insulin signaling pathway. The researchers found that sleep deprivation caused a 30% reduction in insulin response in the adipose tissue in sleep deprived study participants when compared to well rested study participants.
The authors wrote, “We observed an approximate 30% reduction of cellular insulin sensitivity in adipocytes from subcutaneous fat samples collected in healthy, young, lean adults after 4 nights of sleep restriction compared with 4 nights of normal sleep in a randomized, crossover study. Phosphorylation of Akt, a crucial step of the phosphatidylinositol 3-kinase (PI3K) pathway that mediates most metabolic actions of insulin, was markedly impaired after sleep restriction”.
The authors also wrote, “… 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…. 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”.
The authors suggest that sleep deprivation may be involved in the etiology of obesity and type 2 diabetes when they wrote, “The approximate 30% reduction in cellular insulin signaling in adipocytes induced by 4 nights of sleep restriction lies within the range of the difference in insulin sensitivity in adipocytes from obese versus lean participants and from diabetic patients versus nondiabetic participants”.
The authors concluded, “… our finding of a robust alteration in intracellular insulin signaling in a peripheral tissue that is pivotal in regulating energy balance and metabolism identifies a molecular mechanism underlying the adverse effect of sleep disturbances on insulin sensitivity”.
In an accompanying editorial, it was commented that “…Broussard and colleagues’ study substantially challenges the traditional views that the primary purpose of sleep is confined to restorative effects on the central nervous system. These results point to a much wider influence of sleep on bodily functions, including metabolism, adipose tissue, cardiovascular function, and possibly more”.
This study is quite remarkable and identifies a molecular mechanism where sleep deprivation can influence the response of fat cells to insulin. In prolonged sleep deprivation, the response seen in this paper can lead to prediabetes, type 2 diabetes, and possibly obesity. This study is small in size and will need to be reproduced on a larger scale. In addition, less severe sleep deprivation which occurs in the general population should be studied. In today’s society that runs of a 24 hour basis, the findings of this study could have public health implications for the treatment of prediabetes, type 2 diabetes, and obesity.
Josiane L. Broussard et al. “Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study” Ann Intern Med. October 16, 2012; 157(8):549-557