Summary
Dr. Christie Ballantyne, lead investigator of a study linking obesity and asthma, says patients who lost weight saw decreased levels of eotaxin -- an inflammatory mediator known to play a key role in asthma flare-ups -- meaning weight loss may be a very effective therapy for treating asthma sufferers.
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Details
Research presented at the American Diabetes Association's Scientific Sessions today 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.
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.
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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