Understanding Obesity: New research examines how hunger signals work in
the brain
April 14, 2003
Saint Louis University study suggests new approach to treating obesity
Obese people are not getting critical chemical signals to their brains
that tell them to stop eating, findings from Saint Louis University suggest.
The review of research was published in the March issue of Current
Pharmaceutical Design.
Normally, a protein called leptin is released from fat cells and hitches
a ride across the blood vessels that feed the brain, known as the
"blood-brain barrier." The protein then is in the right place to tell the
brain that the body has had enough to eat, to eat less or to burn calories
faster.
However, among those who are obese, the brain doesn't seem to be getting
the message. This could be because the blood-brain barrier doesn't properly
transport the leptin or because the brain isn't interpreting the signals
properly.
William A. Banks, M.D., professor of geriatrics in the department of
internal medicine and professor of pharmacological and physiological science
at Saint Louis University School of Medicine, speculates that people gain
fat to increase the amount of leptin needed to push through the
communications bottleneck.
"The research is significant as its suggests a new way that the brain and
the body communicate about body weight. Obesity is the result when that
communication falters," he says. Banks, who is also a staff physician at
Veterans Affairs Medical Center in St. Louis, says problems with
transporting leptin to the brain lead to a vicious cycle.
Obesity apparently triggers a mechanism that prevents signals to stop
eating from getting to the brain, which leads to more obesity. And as
obesity increases, the likelihood decreases of the signals getting through.
"The problem with communicating across the blood-brain barrier comes with
increasing obesity and increasing obesity makes it more difficult for the
brain and body to communicate about weight. Our research found that fat mice
get fatter as they age and skinny ones stay about the same," he says.
"Fat mice develop a blood-brain barrier defect but skinny ones don't. To
some degree, that defect is reversible with weight loss."
Animals are not born with communications signals blocked between the body
and brain. The problem develops with time, Banks says.
"Maybe some environmental factor or substance from within the body
triggers this. Substances such as epinephrine can stimulate transporting
leptin into the brain. Conversely, there might be substances that impair
transporting leptin. If we could identify them, we could develop a new
treatment for obesity based on blocking the substances that prevent leptin
from getting into the brain."
Saint Louis University
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