U.S. Department of Health and Human Services
NIH News
National Institutes of Health
Study Finds Possible Mechanism for Link
Between Sleep Disturbances and Metabolic Syndrome
April 21, 2005 -
A new mouse study suggests that a brain system that
controls the sleep/wake cycle might also play a role in
regulating appetite and metabolism. Mice with a mutation in a
gene called "Clock," which helps drive circadian rhythm, ate
significantly more and gained more weight. The finding could
help explain why disrupted sleep patterns – particularly when
combined with a high-fat diet – are associated with excessive
weight gain and the onset of metabolic syndrome in some people,
according to investigators supported by the National Institutes
of Health (NIH).
The study, by Fred W. Turek, Ph.D., and Joseph Bass, M.D.,
Ph.D., of Northwestern University in Evanston, Ill., and others
will be available at the Science Express website,
on April 21, 2005. The National Institute on Aging (NIA), the
National Heart, Lung and Blood Institute (NHLBI), and the
National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK) supported this work. The NIA, NHLBI and NIDDK are
components of the NIH at the U.S. Department of Health and Human
Services.
At least 40 million Americans have chronic sleep problems, and
an additional 20 million experience occasional sleeping
problems. As many as 47 million Americans have metabolic
syndrome, a cluster of conditions shown to increase a person's
risk of heart disease and stroke. The National Cholesterol
Education Program defines metabolic syndrome as having at least
3 of the following risk factors: high blood pressure, high
glucose (sugar) levels which can indicate risk for diabetes,
high triglyceride levels, low levels of good cholesterol, and a
large waist.
Scientists have found that circadian rhythms (which control the
sleep/wake cycle and other biological processes), hunger, and
satiety are all regulated by centers within a brain structure
called the hypothalamus. And previous studies in humans have
suggested that disrupted sleep patterns may contribute to the
development of obesity, diabetes, and metabolic syndrome.
In this latest work, Turek and his colleagues found that mutant
mice were more active during times when rodents usually sleep.
They also had less fluctuation in blood levels of leptin, a
hormone that transmits a satiety signal to the brain. The
researchers also found that Clock mutant mice had reduced levels
of the hormone ghrelin within the hypothalamus, indicting that
ghrelin may participate in the neuronal relay linking sleep,
wakefulness, and appetite. Together, these alterations in neural
and peripheral hormones suggest that a number of previously
undetected brain circuits may exist that are common to sleep and
eating.
The mice with a mutation in the Clock gene fed a regular diet
gained about as much weight as normal mice that were fed a
high-fat diet. The mice with a mutation in the Clock gene showed
even greater weight gain and changes in metabolism when fed a
high-fat diet. They developed a wide range of conditions
associated with obesity, diabetes, and the metabolic syndrome,
such as high levels of blood cholesterol, triglycerides, and
glucose, and insulin resistance.
Andrew Monjan, Ph.D., of the NIA and Carl E. Hunt, M.D.,
director of the NIH National Center on Sleep Disorders Research,
are available to discuss this study. To arrange an interview
with Dr. Monjan, phone (301) 496-1752; for Dr. Hunt, phone (301)
496-4236.
NIA, NHLBI, and NIDDK are part of the National Institutes of
Health (NIH), the Federal Government's primary agency for
biomedical and behavioral research. NIH is a component of the
U.S. Department of Health and Human Services. NIA information on
conditions and diseases associated with aging is available at www.nia.nih.gov. NHLBI press releases and fact sheets, including
information on obesity and sleep disorders can be found online
at www.nhlbi.nih.gov. NIDDK information on weight control and
nutrition can be found online at www.niddk.nih.gov.
Click here to read about
Guidelines for Metabolic Syndrome
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