Too little sleep may fuel insulin resistance

People who consistently get too little sleep face bigger concerns than daytime fatigue and crankiness. Over the long term, sleep deprivation also increases the risk of serious health problems including obesity and type II diabetes.

Scientists have come up with a number of plausible explanations for this increased risk. Various studies have shown, for instance, that how much we sleep can affect blood sugar levels, hormones that control appetite, and even the brain's perception of high-calorie foods.

A small new study, published Monday in the Annals of Internal Medicine, adds a key piece to the puzzle by drilling down to the cellular level: Sleep deprivation, the study found, impairs the ability of fat cells to respond to insulin, a hormone that regulates metabolism and is involved in diabetes.

In the study, seven healthy young men and women spent a total of eight days and nights in a sleep lab. They were allowed to sleep normally on four of the nights, and on the other nights they were limited to just 4.5 hours. In order to neutralize the effects of appetite or overeating, the researchers strictly controlled the participants' meals and calorie intake.

After the four nights of sleep deprivation, blood tests revealed that the participants' overall insulin sensitivity was 16% lower, on average, than after the nights of normal sleep. Moreover, their fat cells' sensitivity to insulin dropped by 30%, to levels typically seen in people who are obese or who have diabetes.

"This is the equivalent of metabolically aging someone 10 to 20 years just from four nights of partial sleep restriction," says Matthew Brady, the senior author of the study and an associate professor of medicine at the University of Chicago. "Fat cells need sleep, and when they don't get enough sleep, they become metabolically groggy."

Specifically, the participants' fat cells -- which were collected via biopsy and analyzed -- required nearly three times as much insulin to activate an enzyme known as Akt, which plays a crucial role in regulating blood sugar. If insulin resistance of this sort becomes persistent, excess sugar and cholesterol can accumulate in the blood, increasing the risk of diabetes and heart disease.

Previous sleep-lab studies have found that insufficient sleep can affect overall insulin sensitivity, but this is the first to identify a concrete cellular mechanism that might underlie the well-established links between sleep, diabetes and obesity.

"This takes the research on the effect of sleep deprivation on metabolism one step further, by revealing a molecular mechanism involved in the reduction of total body insulin sensitivity," says Dr. Nathaniel F. Watson, co-director of the University of Washington Medicine Sleep Center, in Seattle, who was not involved in the study.

"If you want to make a causal argument that short sleep is causing diabetes," Watson adds, "one of the key elements is coming up with a physiological mechanism by which this would happen."