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Eotaxin and other inflammatory mediators may link obesity to
asthma, and targeting adiposity/eotaxin may have benefit in obese asthmatics.
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Research presented at the American Diabetes Association's
Scientific Sessions showed that therapies targeting
abdominal fat tissue, such as weight loss, may provide a new
approach to treat asthma.
"The incidence of asthma and obesity is increasing worldwide, and
asthma is often more severe in the obese," said Dr. Christie
Ballantyne, lead investigator of the study and director of the
Center for Cardiovascular Disease Prevention at the Methodist
DeBakey Heart Center in Houston. "We found that fat tissue inside of
the abdomen is an important source of eotaxin, which is an
inflammatory mediator that is known to play a key role in asthma. "
According to research conducted by Dr. Ballantyne, obese
patients' eotaxin levels were significantly reduced with weight
loss. This finding is important because it may provide physicians
and patients with a new approach to treat this debilitating
disorder.
Methodology
The relation between eotaxin and obesity was studied in mice fed
a high-fat diet and in obese humans. Circulating eotaxin levels were
compared in obese vs. lean mice, obese humans vs. lean humans, and
obese humans before and after weight loss. Eotaxin mRNA levels were
compared in fat tissue from obese vs. lean mice and in subcutaneous
vs. visceral fat tissue from patients undergoing bariatric surgery.
Eotaxin levels were significantly higher in obese mice than lean
mice, and mRNA levels in the fat tissue were positively correlated
with serum levels of eotaxin. In obese patients, plasma eotaxin
levels were significantly higher (82.6„b5.0 vs. 44.5„b6.08 pg/ml in
lean controls; p=0.004) and significantly reduced after weight loss
(62.8„b4.0 pg/ml; p<0.001), and eotaxin mRNA levels were 4.7-fold
higher in visceral than in subcutaneous adipose tissue (p=0.008).

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Circulating eotaxin levels are increased in diet-induced obesity
in both mice and humans, and eotaxin mRNA levels were high in
visceral adipose tissue in both species. Diet-induced weight loss in
humans led to a reduction in plasma eotaxin levels, demonstrating
that clinical interventions that target obesity can modulate
systemic eotaxin levels.
This shows that eotaxin and other inflammatory mediators may link
obesity to asthma, and targeting adiposity/eotaxin may have benefit
in obese asthmatics.
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Sources
The study was presented on Sunday
June 12 during the 6:30-7:30PM poster session.
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