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(16-12-12) Even Your Fat Cells Need Sleep, According to New Research



(courtesy of the National Sleep Foundation)

In a study that challenges the long-held notion that the primary function of
sleep is to give rest to the brain, researchers have found that not getting
enough shut-eye has a harmful impact on fat cells, reducing by 30 percent their
ability to respond to insulin, a hormone that regulates energy.

Sleep deprivation has long been associated with impaired brain function,
causing decreased alertness and reduced cognitive ability. The latest finding ?
published by University of Chicago Medicine researchers in the Oct. 16 issue of
the Annals of Internal Medicine ? is the first description of a molecular
mechanism 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. The study suggests that sleep?s role in energy metabolism is
at least 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.

Brady said 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.?

Esra Tasali, MD, assistant professor of medicine at the University of Chicago
and co-senior author, led the recruitment of six men and one woman, all young,
lean and healthy. Each volunteer went through two study conditions, 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.
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.

After four nights of short sleep, total-body insulin response decreased by an
average of 16 percent. 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.

They 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.

?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.?

The study was one of the first to bring together sleep research experts and
biologists focused on energy regulation and metabolism in adipose tissue. The
impetus came from a sleep-research graduate student, Josiane Broussard, PhD ?
10, lead author of the study and now a Society in Science-Branco Weiss fellow
at Cedars-Sinai Medical Center in Los Angeles. She wanted to combine her
interest in sleep and metabolism with research at the molecular level.

So she pulled together a team for this project that included the two sleep
researchers, Tasali and Van Cauter, plus two specialists from the University of
Chicago Kovler Diabetes Center, David Ehrmann, MD, and Brady, who studies how
insulin regulates energy storage in fat and liver cells.

They focused on fat cells because of their direct links to metabolic
disruption and weight gain. These cells store energy for the body, are
exquisitely sensitive to insulin and help regulate appetite.

Witnessing the direct effect of sleep deprivation on a peripheral tissue such
as fat at the cellular level ?was an eye-opener,? Broussard said. 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.?

Brady said the study opens up many new questions.

?What signals from sleep loss affect the fat cell? What effect does
dysfunctional fat have at the whole-body level?? Brady wondered. ?And if we can
deprive healthy people of sleep and make them worse, can we take sick people,
such as those with the common combination of sleep apnea, obesity and diabetes,
improve their sleep and make them better? That?s the missing link in the sleep-
obesity-diabetes connection.?

This study is ?a valuable contribution to the understanding of the causal
pathways by which reduced sleep duration may directly contribute to diabetes
and obesity,? according to an editorial in the journal by Francesco Cappuccio,
MD, DSc, and Michelle Miller, PhD, of the University of Warwick, in Coventry,
United Kingdom. ?These results point to a much wider influence of sleep on
bodily functions, including metabolism, adipose tissue, cardiovascular
function, and possibly more.?

SOURCE: www.johnnybowden.com

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