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Research linking obesity and asthma shows weight reduction may provide therapy for asthma sufferers
June 13, 2005Saturday, June 11, 2005 (San Diego) - 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).
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.
The Methodist Hospital
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).
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.
The Methodist Hospital
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