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Understanding Obesity: New Research Examines How Hunger Signals Work In The Brain

Date:
April 10, 2003
Source:
Saint Louis University
Summary:
Obese people are not getting critical chemical signals to their brains that tell them to stop eating, findings from Saint Louis University suggest.
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ST. LOUIS -- 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."

Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first M.D. degree west of the Mississippi River. Saint Louis University School of Medicine is a pioneer in geriatric medicine, organ transplantation, chronic disease prevention, cardiovascular disease, neurosciences and vaccine research, among others. The School of Medicine trains physicians and biomedical scientists, conducts medical research, and provides health services on a local, national and international level.


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The above post is reprinted from materials provided by Saint Louis University. Note: Materials may be edited for content and length.


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Saint Louis University. "Understanding Obesity: New Research Examines How Hunger Signals Work In The Brain." ScienceDaily. ScienceDaily, 10 April 2003. <www.sciencedaily.com/releases/2003/04/030410071927.htm>.
Saint Louis University. (2003, April 10). Understanding Obesity: New Research Examines How Hunger Signals Work In The Brain. ScienceDaily. Retrieved September 1, 2015 from www.sciencedaily.com/releases/2003/04/030410071927.htm
Saint Louis University. "Understanding Obesity: New Research Examines How Hunger Signals Work In The Brain." ScienceDaily. www.sciencedaily.com/releases/2003/04/030410071927.htm (accessed September 1, 2015).

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