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Swim training improves leptin receptor deficiency-induced obesity and lipid disorder by activating uncoupling proteins

Authors
Oh, Ki SookKim, Eun YoungYoon, MichungLee, Chung Moo
Issue Date
Jun-2007
Publisher
NATURE PUBLISHING GROUP
Keywords
adipose tissue; white; leptin receptor; lipid metabolism disorders; mitochondrial uncoupling protein; obesity
Citation
EXPERIMENTAL AND MOLECULAR MEDICINE, v.39, no.3, pp 385 - 394
Pages
10
Journal Title
EXPERIMENTAL AND MOLECULAR MEDICINE
Volume
39
Number
3
Start Page
385
End Page
394
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/14675
DOI
10.1038/emm.2007.43
ISSN
1226-3613
2092-6413
Abstract
Leptin receptor deficiency causes morbid obesity and hyperlipidemia in mice. Since physical exercise enhances energy expenditure, it is an important part of successful weight-control regimens. We investigated the mechanism by which swim training regulates leptin receptor deficiency-induced obesity and lipid disorder in a mouse model of obesity (obese db/db mouse). Swim training for 6 weeks significantly decreased body weight gain and adipose tissue mass in both sexes of obese and lean mice, compared to their respective sedentary controls. These effects were particularly evident in obese mice. Swim training also caused significant decreases in serum levels of triglycerides, free fatty acids and total cholesterol in both obese and lean mice. In obese mice, swim training increased the levels of mRNAs and proteins encoding uncoupling protein 1 (UCP1), UCP2 and UCP3 in brown adipose tissue, white adipose tissue and skeletal muscle, respectively. In conclusion, these findings suggest that, in mice, swim training can effectively prevent body weight gain, adiposity and lipid disorders caused by leptin receptor deficiency, in part through activation of UCPs in adipose tissue and skeletal muscle, which may contribute to alleviating metabolic syndromes, such as obesity, hyperlipidemia and type 2 diabetes.
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