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Senior Citizen Health & Medicine
Researchers Think Stress Makes Us Obese and They
Know How to Stop It
Discovery provides key to manipulate fat in specific
parts of body
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Investigators used
simple, nontoxic chemical injections to add and
remove fat in targeted areas on the bodies of mice. |
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July 2, 2007 – When two people eat the same diet
and one gains weight and the other does not, it may be stress causing
the weight gain. At least that is what researchers have found in mice.
Stressed mice gained twice as much fat as unstressed mice on the same
diet. Researchers say a molecule released in the body by stress is to
blame and this finding may provide a way to prevent obesity.
Some have suggested this may offer some light on
the obesity epidemic that has struck the U.S. The theory being that
people are more stressed today than in past years, thus are gaining more
weight. Stress has also recently been linked to another growing concern
– Alzheimer’s disease.
In what they call a “stunning research advance,”
investigators at Georgetown University Medical Center have gone even
further with their new knowledge to use simple, non-toxic chemical
injections to add and remove fat in targeted areas on the bodies of
laboratory animals.
They say the discovery, published online in Nature
Medicine on July 1, could revolutionize human cosmetic and
reconstructive plastic surgery and treatment of diseases associated with
human obesity.
Investigators say these findings may also, over the
long-term, lead to better control of metabolic syndrome, which is a
collection of risk factors that increase a patient’s chances of
developing heart disease, stroke, and diabetes. Sixty million Americans
were estimated to be affected by metabolic syndrome in 2000, according
to a study funded by the Centers for Disease Control in 2004.
In the paper, the Georgetown researchers describe a
mechanism they found by which stress activates weight gain in mice, and
they say this pathway − which they were able to manipulate − may explain
why people who are chronically stressed gain more weight than they
should based on the calories they consume.
This pathway involves two players − a
neurotransmitter (neuropeptide Y, or NPY) and the receptor (neuropeptide
Y2 receptor, or Y2R) it activates in two types of cells in the fat
tissue: endothelial cells lining blood vessels and fat cells themselves.
In order to add fat selectively to the mice they tested, researchers
injected NPY into a specific area.
The researchers found that both NPY and Y2R are
activated during stress, leading to apple-shape obesity and metabolic
syndrome. Both the weight gain and metabolic syndrome, however, were
prevented by administration of Y2R blocker into the abdominal fat.
“We couldn’t believe such fat remodeling was
possible, but the numerous different experiments conducted over four
years demonstrated that it is, at least in mice; recent pilot data also
suggest that a similar mechanism exist in monkeys as well,” said the
study’s senior author, Zofia Zukowska, M.D., Ph.D., professor and chair
of the Department of Physiology & Biophysics at Georgetown University
Medical Center.
“We are hopeful that these findings might
eventually lead to control of metabolic syndrome, which is a huge health
issue for many Americans,” she said. “Decreasing fat in the abdomen of
the mice we studied reduced the fat in their liver and skeletal muscles,
and also helped to control insulin resistance, glucose intolerance,
blood pressure and inflammation. Blocking Y2R might work the same way in
humans, but much study will be needed to prove that.”
More immediately, the findings could provide some
comfort to stressed individuals who blame themselves for a weight gain
that seems outsized given the food they eat, said Lydia Kuo, a medical
student who earned her Ph.D. in physiology due to work on the study.
“This is the first study to show that stress has a
direct effect on fat accumulation, body weight and metabolism,” she
said. “In humans, this kind of stress-mediated fat gain may have nothing
to do with the brain, and is actually just a physiological response of
their fat tissue.”
And perhaps the most rapid clinical application of
these results will be in both cosmetic and reconstructive plastic
surgery, said co-author Stephen Baker, M.D., D.D.S, associate professor
of plastic surgery at Georgetown University Hospital. The ability to add
fat as a graft would be useful for facial rejuvenation, breast surgery,
buttock and lip enhancement, and facial reconstruction, he said, and
using injections like those tested in this study could make fat grafts
predictable, inexpensive, biocompatible and permanent.
Equally important, blocking Y2R resulted in local
elimination of adipose, or fat, tissue, said Baker. “This is the first
well-described mechanism found that can effectively eliminate fat
without using surgery,” he said. “A safe, effective, non-surgical means
to eliminate undesirable body fat would be of great benefit to our
patients.”
Roxanne Guy, MD, president of the American Society
of Plastic Surgeons, of which Baker is a member, is also excited by the
findings, although she agrees that more research is needed to find out
how the animal findings translate in humans. “Providing a long lasting,
natural wrinkle filler and a scientifically studied, non-surgical method
for melting fat could revolutionize ‘growing old gracefully,’” she said.
“This discovery could also have positive implications for reconstructive
plastic surgery procedures performed on the face and breasts.”
Stress + “comfort” foods = excess weight gain
As part of the study, Zukowska and her team
examined the effect of several forms of chronic stress that mice in the
wilderness can encounter, such as exposure for an hour a day over a
two-week period to standing in a puddle of cold water or to an
aggressive alpha mouse, and they conducted the experiments in
combination with a regular diet or with a high-fat, high-sugar diet.
Stressed animals fed a normal diet did not gain weight, but stressed
mice given a high-fat diet did. In fact, the researchers found these
mice put on more weight than expected given the calories they were
consuming.
“They gained twice as much fat as would be
expected, and it was all in their belly area,” Kuo said. Stressed versus
non-stressed animals ate the same amount of food, but the stressed
animals processed it differently, she said, explaining, “the novel
finding here is that NPY works on fat tissue, not in the brain.”
This finding makes sense if evolutionary advantage
is considered, Zukowska said. “If you can store fat for times of
hardship, you have a fat reserve that can be turned into energy for the
next fight.
“The same mechanism may be happening in humans,”
she said. “An accumulation of chronic stressors, like disagreements with
your boss, taking care of a chronically ill child, or repeated traffic
road rages, could be acting as an amplifier to a hypercaloric diet when
protracted over time. Depression may also be acting as a stressor.”
Not only were the stressed mice much fatter, they
began to exhibit the metabolic and cardiovascular consequences of
obesity, Kuo said. “They had the glucose intolerance seen in diabetes,
elevated blood pressure, inflammation in the blood vessels, and fat in
their livers and muscles.”
“Although we don’t expect that, in the future, a
person will be able to eat everything he or she wants, chase it down
with a Y2R blocking agent, and end up looking like a movie star,” said
Zukowska, “we are encouraged that these findings could improve human
health.”
“The concepts described in this study might give us
the tools to design one method to remodel fat and another to tackle
obesity and metabolic syndrome,” Baker said. “It is very exciting.”
Editor’s Notes:
The study was funded by National Institutes of
Health grants awarded to Zofia Zukowska, a Predoctoral Mid-Atlantic
Fellowship to Lydia Kuo from the American Heart Association, a contract
from the Slovak Research and Development Agency to co-author Richard
Kvetnansky, and grants from National Institutes of Health and the
Plastic Surgery Educational Foundation awarded to a co-author Stephen B.
Baker.
Co-authors include Lydia E. Kuo, Ph.D., Joanna B.
Kitlinska, Ph.D., Jason U. Tilan, M.S., Lijun Li, M.D., Stephen B.
Baker, M.D., DDS, Michael D. Johnson, Ph.D., all from Georgetown
University, Edward W. Lee, M.D., PhD, from the University of
California-Los Angeles, Mary Susan Burnett, Ph.D., from Washington
Hospital Center, Stanley T. Fricke, Ph.D., from Georgetown University,
Richard Kvetnansky Ph.D., from Slovak Academy of Sciences, Bratislava,
Slovakia, Herbert Herzog, Ph.D. from Garvan Insitute, Sydney, Australia,
and Zofia Zukowska, M.D., Ph.D. from Georgetown University.
About Georgetown University Medical Center
Georgetown University Medical Center is an
internationally recognized academic medical center with a three-part
mission of research, teaching and patient care (through our partnership
with MedStar Health). Our mission is carried out with a strong emphasis
on public service and a dedication to the Catholic, Jesuit principle of
cura personalis -- or "care of the whole person." The Medical Center
includes the School of Medicine and the School of Nursing and Health
Studies, both nationally ranked, the world-renowned Lombardi
Comprehensive Cancer Center and the Biomedical Graduate Research
Organization (BGRO).
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