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Mechanism
of Obesity Hormone Revealed
NEW
YORK (Reuters Health) - In the past decade, researchers discovered
a hormone that helped explain why some people could put their
fork down after eating a plate of pasta, while others could go
back for seconds and thirds without ever feeling full.
Subsequent
studies added weight to the role of leptin, a hormone stored primarily
in fat cells, in decreasing appetite, lowering the body's ability
to store fat and boosting the body's ability to burn fat. But
exactly how the ``obesity hormone'' worked has remained a mystery.
Now, a study
in the May 24th issue of Nature reveals that leptin targets multiple
nerve sites and affects the brain in more complex ways than previously
believed. The preliminary findings in mice could pave the way
for the development of drugs to treat obesity and, on the other
end of the weight spectrum, anorexia nervosa, according to lead
author Dr. Malcolm J. Low of Oregon Health Sciences University
in Portland.
``A better
understanding of the fundamental control of appetite and metabolism
by neurons in the hypothalamus will lead to more specific and
efficacious means to stimulate feeding and improve nutrition in
patients with anorexia illness,'' he explained.
Drugs could
also be developed to reverse leptin resistance in obese individuals,
Low said. In many cases, obesity is associated with a resistance
to the effects of leptin in the same way that type 2 diabetes
is caused by a resistance to the hormone insulin, he told Reuters
Health.
In this study,
Low's team found that in mice, leptin activates brain cells called
proopiomelanocortin neurons and also binds to receptors on a second
type of cell.
``This duel
mechanism of leptin action on two interconnected types of neurons
was previously unknown,'' Low said in an interview with Reuters
Health. This mechanism may be an important part of the brain's
ability to maintain a balance among ``long-term body weight, short-term
energy demands, appetite, motivation to seek out food supplies,
and feeding behavior,'' he added.
SOURCE:
Nature 2001;411:480-484.
Reference
Source 89
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