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http://www.sciencedaily.com/releases/2011/05/
110503132704.htm
Turning 'Bad' Fat Into 'Good': A Future Treatment for Obesity?
By knocking down the expression of a protein in rat brains known to stimulate
eating, researchers say they not only reduced the animals' calorie intake and
weight, but also transformed their fat into a type that burns off more energy.
(Credit: © Otto Durst / Fotolia)
ScienceDaily (May 3, 2011) By knocking down the expression of a protein in
rat brains known to stimulate eating, Johns Hopkins researchers say they not
only reduced the animals' calorie intake and weight, but also transformed their
fat into a type that burns off more energy. The finding could lead to better
obesity treatments for humans, the scientists report.
"If we could get the human body to turn 'bad fat' into 'good fat' that burns
calories instead of storing them, we could add a serious new tool to tackle the
obesity epidemic in the United States," says study leader Sheng Bi, M.D., an
associate professor of psychiatry and behavioral sciences at the Johns Hopkins
University School of Medicine.
More than two-thirds of adults in the United States are overweight, and more
than one-third are obese, according to government estimates.
The Johns Hopkins study, published in the journal Cell Metabolism, looks at two
types of fat made by the body: white and brown adipose tissue. White fat is the
typical fat that ends up around your middle and other places, and is the
storehouse for the extra calories we eat. White fat cells have a single large
droplet of lipid, one of fat's building blocks, such as cholesterol and
triglycerides.
Cells in brown fat, considered a "good fat" for its energy-burning qualities,
contain many little droplets of lipid, each with its own power source, which
enables heat generation. Babies have ample stores of brown fat at birth as a
defense against the cold, but it mostly disappears, as adults have very little
of this calorie-burning tissue.
Bi and his colleagues designed an experiment to see if suppressing the
appetite-stimulating neuropeptide Y (NPY) protein in the dorsomedial
hypothalamus of the brain would decrease body fat in rats. Located just above
the brain stem, the hypothalamus helps regulate thirst, hunger, body
temperature, water balance and blood pressure.
For five weeks, two groups of rats were fed a regular diet, with one group also
treated with a virus to inhibit NPY expression and the other left as a control
group. At the end of five weeks, the treated group weighed less than the
control group, demonstrating that suppression of NPY reduced eating.
Then, researchers split each of the groups into two, creating four sets of
rats. One of the treated groups of rats and one of the control groups were fed
a regular diet while the other treated and control groups got a high-fat diet.
Of the rats on the regular diet, the control group weighed more at the end of
11 weeks than those rats in which hypothalamic NPY expression was knocked down.
In the high-fat group, the control group rats became obese; those rats in which
NPY expression was silenced gained less weight.
Bi says the results "made sense," given that NPY has been shown to stimulate
eating. The less NPY, the less the rats would eat, his team hypothesized. What
was a surprise, however, was what they found after they checked the fat content
of rats after death. In the groin area of the NPY rats, researchers discovered
not the expected white fat found in adult rats, but the telltale signs of brown
fat in its place. They confirmed this change by looking at levels of
mitochondrial uncoupling protein-1, or UCP-1, through which brown fat burns to
produce heat. They used this protein as a marker to determine that the fat that
should have been white was instead brown.
Bi says he believes that the transformation from white to brown fat resulting
from NPY suppression may be due to activation of brown fat stem cells contained
in white fat tissue. While brown fat seems to vanish in humans as they emerge
from infancy, the brown fat stem cells may never disappear and may just become
inactive as people age.
Bi says it may be possible to transplant or inject brown fat stem cells under
the skin to burn white fat and stimulate weight loss. "Only future research
will tell us if that is possible," he says.
This study also shows that low levels of hypothalamic NPY increase spontaneous
physical activity, improve blood sugar levels and enhance insulin sensitivity
in rats, but it remains undetermined whether this brown fat transformation also
contributes to these effects.
The study was funded by the U.S. National Institute of Diabetes and Digestive
and Kidney Diseases. Along with Bi, other Johns Hopkins researchers involved in
the study include Pei-Ting Chao, Timothy H. Moran, Ph.D., and Susan Aja, Ph.D.
Liang Yang, Ph.D., formerly of Johns Hopkins and now at the Massachusetts
Institute of Technology, also contributed.
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Story Source:
The above story is reprinted (with editorial adaptations by ScienceDaily
staff) from materials provided by Johns Hopkins Medical Institutions, via
EurekAlert!, a service of AAAS.
Journal Reference:
1. Pei-Ting Chao, Liang Yang, Susan Aja, Timothy H. Moran, Sheng Bi.
Knockdown of NPY Expression in the Dorsomedial Hypothalamus Promotes
Development of Brown Adipocytes and Prevents Diet-Induced Obesity. Cell
Metabolism, 2011; 13 (5): 573-583 DOI: 10.1016/j.cmet.2011.02.019
Need to cite this story in your essay, paper, or report? Use one of the
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Johns Hopkins Medical Institutions (2011, May 3). Turning 'bad' fat into
'good': A future treatment for obesity?. ScienceDaily. Retrieved May 5, 2011,
from http://www.sciencedaily.com /releases/2011/05/110503132704.htm
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis
or treatment. Views expressed here do not necessarily reflect those of
ScienceDaily or its staff.
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