Sleep deprivation contributes to obesity and diabetes
A multidisciplinary team at the University of Chicago Medicine (UCM) has shown the first link at the cell level connecting sleep deprivation with a disruption of energy regulation in humans. This finding has important implications relative to two major health risks in modern society, obesity and diabetes.
It challenges a long-held notion that sleep’s primary function is simply to provide rest for the brain. The new study, published in the October 16 issue of Annals of Internal Medicine, demonstrates that sleep’s role in regulating energy metabolism is as critical as its role in brain function. The study was one of the first to bring together sleep research experts and biologists studying energy regulation and metabolism in adipose tissue. It focused on fat cells due to their direct links to metabolic disruption and weight gain. Fat cells store energy, are highly sensitive to insulin and help regulate appetite.
“Many people think of fat as a problem, but it serves a vital function,” says study co-author, Dr. Matthew Brady, vice chair of the Committee on Molecular Metabolism and Nutrition at UCM. “In storage mode, fat cells remove fatty acids and lipids from the circulation where they can damage other tissues. When fat cells cannot respond effectively to insulin, these lipids leach out into the circulation, leading to serious complications.”
Six men and one woman, all young, lean and healthy, participated in the study. Each volunteer went through two study conditions at four-week intervals. First, they spent 8 1/2 hours in bed for four consecutive nights. On the second visit, they spent 4 1/2 hours in bed each night. Food intake was strictly controlled and identical under both conditions.
On the morning after the fourth night following the long and short sleep cycles, each volunteer took an intravenous glucose tolerance test, which measures total-body insulin sensitivity. They also underwent a biopsy that removed abdominal fat cells and measured how these cells responded to insulin.
After four nights of short sleep, total-body insulin response decreased by an average of 16 percent while fat cells’ insulin sensitivity decreased by 30 percent. The reduction is comparable to the difference between cells from obese versus lean participants and diabetic versus nondiabetics.
These findings show that sleep loss, an increasingly common condition in our over-scheduled, 24/7 environment, can lead over time to weight gain, diabetes and other health problems.
“Some people claim they can tolerate the cognitive effects of routine sleep deprivation,” says Dr. Eve Van Cauter, director of the Sleep, Metabolism and Health Center at the university. “In this small but thorough study, however, we found that seven out of seven subjects had a significant change in insulin sensitivity. They are not tolerating the metabolic consequences,” she says.
While the study involved some of the university’s top researchers, the impetus came from a sleep-research graduate student. Josiane Broussard, the study’s lead author and now a Society in Science-Branco Weiss fellow at Cedars-Sinai Medical Center in Los Angeles.
Brady says that Broussard’s “game-changing idea” resulted from her desire to combine her research on sleep and metabolism with human subjects by studying fat tissues at the molecular level in the lab.
“If you had told me before Josiane joined our group that I would be working on a sleep study, I would have shown you the door,” claims Brady. But he has since become a convert to the possibilities of future research in this area.
“And if sleep depriving young, healthy volunteers results in a worsening of their insulin sensitivity, both at the cellular level and systemically, can we take people with metabolic diseases, such as type 2 diabetes, and improve their insulin sensitivity by increasing their sleep quality and/or duration? That’s the missing link in the sleep/obesity/diabetes connection.”