Lack of sleep causing obesity epidemic?

Challenging the long-held notion that the main function of sleep is to give rest to the brain, researchers have found that not getting enough sleep has a significant impact on fat cells, reducing by 30 percent their ability to respond to insulin, a hormone that regulates energy.

The new findings, detailed in the Annals of Internal Medicine, connect sleep loss directly to the disruption of energy regulation in humans, a process that can lead over time to weight gain and diabetes. The researchers suggest that sleep’s role in energy metabolism is at least as important as it is in brain function.

In the study, lean and healthy volunteers were subjected to two conditions, 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. Food intake, strictly controlled, was identical under both study conditions.

On the morning after the fourth night following both the long and short sleep conditions, each volunteer took an intravenous glucose tolerance test, which measures total-body insulin sensitivity. The researchers performed a biopsy, removing abdominal fat cells from the area near each volunteer’s navel. Then they measured 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.

They found that after four nights of short sleep, total-body insulin response decreased by an average of 16 percent and fat cell insulin sensitivity decreased by 30 percent. This reduction is comparable to the difference between cells from obese versus lean participants, or from people with diabetes versus non-diabetic controls.

Additionally, the research team found that the sleep-deprived study participants 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,” notes researcher Esra Tasali, of the University of Chicago.

Co-researcher Matthew Brady, also of the University of Chicago, added that while many people think of fat as a problem, it serves a vital function. “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.”

The study notes that while many people claim to be able to routinely tolerate the cognitive effects of routine sleep deprivation, 100 percent of the study’s subjects exhibited a significant change in insulin sensitivity after the shorter sleep cycle.

Witnessing the direct effect of sleep deprivation on a peripheral tissue such as fat at the cellular level “was an eye-opener,” said co-researcher Josiane Broussard, of the Cedars-Sinai Medical Center. “It helps cement the link between sleep and diabetes and suggests that we could use sleep like diet and exercise to prevent or treat this common disease.”

The results, say the researchers, point to a much wider influence of sleep on bodily functions, including metabolism, adipose tissue, and cardiovascular function. They also raise the intriguing possibility that sick people – such as those with the common combination of sleep apnea, obesity and diabetes – could be treated by simply improving the sufferer’s sleep patterns.

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Source: University of Chicago Medical Center

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