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Study finds molecular link between insufficient sleep, insulin resistance

Researchers find measurable difference in how fat tissue responds to insulin after as little as four nights of restricted sleep

Lack of sleep can change the body’s fat tissue, causing it to behave more like the fat found in an obese or diabetic person, according to a study led by a Cedars-Sinai researcher.

Insufficient sleep has been known to increase the risk of insulin resistance, Type 2 diabetes and obesity, but the study, published by Annals of Internal Medicine in its Oct. 16 issue, identifies the first ever example of an actual metabolic tissue change after sleep deprivation.

“For long term health, you have to protect your sleep,” said Josiane Broussard, PhD, the study’s first author “This study, while small, offers an important clue about the function of sleep and why sleep deprivation leaves us more vulnerable to Type 2 diabetes.”

Even your fat cells require sleep, said Broussard, a fellow at the Cedars-Sinai Diabetes and Obesity Research Institute. In addition to finding a direct connection between sleep loss and disruption of energy regulation in humans, it also challenges the notion that the primary function of sleep is to rest the brain, indicating sleep also plays a role in metabolism.

According to the Centers for Disease Control and Prevention, diabetes affects 25.8 million people in the United States. An estimated 79 million Americans are prediabetic. Diabetes is the seventh leading cause of death in the United States and a major cause of heart disease and stroke.

The clinical study, which was undertaken when Broussard was at the University of Chicago, followed a small number of healthy adults through four days of 4.5 hours in bed and four days of 8.5 hours in bed. The subjects’ diet and level of physical activity were identical regardless of their amount of sleep. After each cycle, researchers took a tissue sample from them for analysis.

After just four nights of sleep restriction, which amounted to just over 14 hours of cumulative sleep loss, the fat tissue samples from the otherwise healthy participants much more closely resembled tissue samples from diabetic or obese subjects. The sleep-deprived participants’ tissue was nearly 30 percent less sensitive to insulin, about the same deficit as that observed in tissue samples from diabetic and obese patients compared to normal healthy adults.

Insulin is a hormone produced by the pancreas that helps the body process sugars. In insulin-resistant patients, the body does not respond appropriately to normal levels of insulin, forcing the pancreas to produce increasing amounts of the hormone to process the same amount of sugar.

The study was one of the first to bring together sleep research experts with biologists focused on energy regulation and metabolism in adipose tissue. Broussard pulled together the team for this project, which included University of Chicago sleep researchers Eve Van Cauter, PhD, Esra Tasali, MD, diabetes specialist David A. Ehrmann, MD, and Matthew J. Brady, PhD, who studies how insulin regulates energy storage in fat and liver cells.

“This eye-opening study helps cement the link between sleep and diabetes, and also suggests that adequate sleep, like diet and exercise, is one of the healthy habits we can adopt to prevent or treat diabetes,” said Broussard, Society in Science—Branco Weiss Fellow at the Cedars-Sinai..

Broussard is continuing her research at Cedars-Sinai, where she is looking at how sleep restriction can affect the body’s organs, cardiac function and blood pressure. Her research fits in well with the goals of the Cedars-Sinai Diabetes and Obesity Research Institute, said Richard Bergman, PhD, the institute’s director.

“Research like this leads us to a better understanding of what factors make us more susceptible to diabetes, obesity and the conditions that lead to them – and bring us another step closer to being able to better predict, prevent, treat and cure these ailments,” Bergman said.

This research for the paper titled “Impaired Insulin Signaling in Human Adipocytes” was supported by National Institutes of Health grants R01-HL086459, 5T32-HL07909, CTSA UL1-RR024999, P60-DK020595, P50 HD-057796, and P01-AG11412 as well as Society in Science through the Branco Weiss Fellowship awarded to Broussard.

Nicole White | Cedars-Sinai News
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