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Old 29-09-2013, 09:25 AM posted to alt.support.diabetes,misc.health.diabetes,alt.food.diabetic
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Default Brain Circuitry That Triggers Overeating Identified

Brain Circuitry That Triggers Overeating Identified


Sixty years ago scientists could electrically stimulate a region of a
mouse’s brain causing the mouse to eat, whether hungry or not. Now,
researchers from UNC School of Medicine have pinpointed the precise
cellular connections responsible for triggering that behavior. The
finding, published in the journal Science, lends insight into a cause
for obesity and could lead to treatments for anorexia, bulimia nervosa
and binge eating disorder, the most prevalent eating disorder in the
United States.

“The study underscores that obesity and other eating disorders have a
neurological basis,” says senior study author Garret Stuber, assistant
professor in the department of psychiatry and department of cell biology
and physiology. He’s also a member of the UNC Neuroscience Center. “With
further study, we could figure out how to regulate the activity of cells
in a specific region of the brain and develop treatments.”

Cynthia Bulik, distinguished professor of Eating Disorders at UNC School
of Medicine and the Gillings School of Global Public Health, says,
“Stuber's work drills down to the precise biological mechanisms that
drive binge eating and will lead us away from stigmatizing explanations
that invoke blame and a lack of willpower.” Bulik was not part of the
research team.

Back in the 1950s, when scientists electrically stimulated a region of
the brain called the lateral hypothalamus, they knew that they were
stimulating many different types of brain cells. Stuber wanted to focus
on one cell type— gaba neurons in the bed nucleus of the stria
terminalis, or BNST. The BNST is an outcropping of the amygdala, the
part of the brain associated with emotion. The BNST also forms a bridge
between the amygdala and the lateral hypothalamus, the brain region that
drives primal functions such as eating, sexual behavior, and aggression.

The BNST gaba neurons have a cell body and a long strand with branched
synapses that transmit electrical signals into the lateral hypothalamus.
Stuber and his team wanted to stimulate those synapses by using an
optogenetic technique, an involved process that would let him stimulate
BNST cells simply by shining light on their synapses.

Typically, brain cells don’t respond to light. So Stuber’s team used
genetically engineered proteins— from algae— that are sensitive to light
and used genetically engineered viruses to deliver them into the brains
of mice. Those proteins then get expressed only in the BNST cells,
including in the synapses that connect to the hypothalamus.

His team then implanted fiber optic cables in the brains of these
specially-bred mice, and this allowed the researchers to shine light
through the cables and onto BNST synapses. As soon as the light hit BNST
synapses the mice began to eat voraciously even though they had already
been well fed. Moreover, the mice showed a strong preference for
high-fat foods.

“They would essentially eat up to half their daily caloric intake in
about 20 minutes,” Stuber says. “This suggests that this BNST pathway
could play a role in food consumption and pathological conditions such
as binge eating.”

Stimulating the BNST also led the mice to exhibit behaviors associated
with reward, suggesting that shining light on BNST cells enhanced the
pleasure of eating. On the flip side, shutting down the BNST pathway
caused mice to show little interest in eating, even if they had been
deprived of food.

“We were able to really home in on the precise neural circuit connection
that was causing this phenomenon that’s been observed for more than 50
years,” Stuber says.

The study, which uses technologies highlighted in the new National
Institutes of Health Brain Initiative, suggests that faulty wiring in
BNST cells could interfere with hunger or satiety cues and contribute to
human eating disorders, leading people to eat even when they are full or
to avoid food when they are hungry. Further research is needed to
determine whether it would be possible to develop drugs that correct a
malfunctioning BNST circuit. Brain

“We want to actually observe the normal function of these cell types and
how they fire electrical signals when the animals are feeding or
hungry,” Stuber says. “We want to understand their genetic
characteristics – what genes are expressed. For example, if we find
cells that become really activated after binge eating, can we look at
the gene expression profile to find out what makes those cells unique
from other neurons.”

And that, Stuber says, could lead to potential targets for drugs to
treat certain populations of patients with eating disorders.

UNC School of Medicine neurobiology graduate student Josh Jennings is
the first author on Stuber’s paper in Science. Authors also include
members of his research team, neurobiology grad student Alice
Stamatakis, research technician Randall Ung, and Giorgio Rizzo of the
University Medical Center Utrecht in the Netherlands.

For this study, Stuber received funding from the National Institute on
Drug Abuse and the Klarman Foundation, a private organization that funds
basic research related to eating disorders.

Source: UNC Health Care

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Old 29-09-2013, 12:10 PM posted to alt.support.diabetes,misc.health.diabetes,alt.food.diabetic
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Default Brain Circuitry That Triggers Overeating Identified

Brain Circuitry That Triggers Overeating Identified

amazing mouse movie :


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