Less Sleep Has Harmful Impact on Fat Cells and Insulin Regime
Sleep deprivation has long been associated with impaired brain function. This not only decreases the alertness but also reduces the cognitive ability.
But the latest study is the first one to give a description of a molecular mechanism that is directly connecting sleep loss to the disruption of energy regulation in humans a process that can lead over time to weight gain, diabetes and other health problems
According to the study conducted by the researchers at the University of Chicago Medicine, lack o sleep has a harmful impact on fat cells thereby reducing 30 percent of the ability to respond to insulin.
Insulin has a profound effect on metabolism. It causes cells in the liver, muscle, and fat tissue to take up glucose from the blood, storing it as glycogen in the liver and muscle, and stopping use of fat as an energy source.
The study highlight the fact that sleep's role in energy metabolism is atleast as important as it is in brain function.
"We found that fat cells need sleep to function properly," said study author Matthew Brady, PhD, associate professor of medicine and vice-chair of the Committee on Molecular Metabolism and Nutrition at the University of Chicago.
According to Brady, body fat plays an important role in humans.
"Many people think of fat as a problem, but it serves a vital function," he said. "Body fat, also known as adipose tissue, stores and releases energy. 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."
For the study six men and one woman, all young, lean and healthy were recruited. This was led by Esra Tasali, MD, assistant professor of medicine at the University of Chicago and co-senior author. Each subject was given two study conditions for at least four weeks apart. In one, they spent 8.5 hours a night in bed for four consecutive nights. In the other, they spent 4.5 hours in bed for four nights. They researchers made sure that the food intake, strictly controlled, was identical under both study conditions.
On the 5th day after the long and short sleep conditions, the subjects were made to take an intravenous glucose tolerance test, which measures total-body insulin sensitivity. Following which a biopsy was done by the researchers removing abdominal fat cells from the area near each volunteer's navel. Then analyzed how these fat cells responded to insulin.
The researchers assessed insulin sensitivity at the molecular level by measuring the phosphorylation of a protein called Akt within fat cells. Akt phosphorylation is a crucial early chemical step in the cell's response to insulin.
The total body insulin response decreased by an average of 16 percent after four nights of short sleep. The insulin sensitivity of fat cells decreased by 30 percent. This reduction is comparable to the difference between cells from obese vs. lean participants or from people with diabetes versus non-diabetic controls.
Plus the sleep deprived subjects had a decreased response to a range of doses of insulin. It took nearly three times as much insulin to provoke half of the maximum Akt response in volunteers who had been deprived of sleep.
"Sleeping four to five hours a night, at least on work days, is now a common behavior" said study author and sleep specialist Esra Tasali.
"Some people claim they can tolerate the cognitive effects of routine sleep deprivation," said co-author Eve Van Cauter, PhD, the Frederick H. Rawson Professor of Medicine and director of the sleep, metabolism and health center at the University of Chicago. "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."
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