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1.
Nutrition Research and Practice ; : 198-204, 2011.
Article in English | WPRIM | ID: wpr-40493

ABSTRACT

Target herbal ingredient (THI) is an extract made from two herbs, Scutellariae Radix and Platycodi Radix. It has been developed as a treatment for metabolic diseases such as hyperlipidemia, atherosclerosis, and hypertension. One component of these two herbs has been reported to have anti-inflammatory, anti-hyperlipidemic, and anti-obesity activities. However, there have been no reports about the effects of the mixed extract of these two herbs on metabolic diseases. In this study, we investigated the metabolic effects of THI using a diet-induced obesity (DIO) mouse model. High-fat diet (HFD) mice were orally administered daily with 250 mg/kg of THI. After 10 weeks of treatment, the THI-administered HFD mice showed reduction of body weights and epididymal white adipose tissue weights as well as improved glucose tolerance. In addition, the level of total cholesterol in the serum was markedly reduced. To elucidate the molecular mechanism of the metabolic effects of THI in vitro, 3T3-L1 cells were treated with THI, after which the mRNA levels of adipogenic transcription factors, including C/EBPalpha and PPARgamma, were measured. The results show that the expression of these two transcription factors was down regulated by THI in a dose-dependent manner. We also examined the combinatorial effects of THI and swimming exercise on metabolic status. THI administration simultaneously accompanied by swimming exercise had a synergistic effect on serum cholesterol levels. These findings suggest that THI could be developed as a supplement for improving metabolic status.


Subject(s)
Animals , Mice , 3T3-L1 Cells , Adipose Tissue, White , Atherosclerosis , Body Weight , Cholesterol , Diet, High-Fat , Flavonoids , Glucose , Hyperlipidemias , Hypertension , Metabolic Diseases , Obesity , PPAR gamma , RNA, Messenger , Scutellaria baicalensis , Swimming , Transcription Factors , Weights and Measures
2.
Experimental & Molecular Medicine ; : 385-394, 2007.
Article in English | WPRIM | ID: wpr-201415

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.


Subject(s)
Animals , Female , Male , Mice , Adipose Tissue/metabolism , Body Weight , Ion Channels/genetics , Lipid Metabolism , Mitochondrial Proteins/genetics , Muscle, Skeletal/metabolism , Obesity/genetics , Physical Conditioning, Animal , RNA, Messenger/metabolism , Receptors, Cell Surface/deficiency , Receptors, Leptin , Swimming
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