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BioFactors 2008

Lipid profile lowering effect of Soypro fermented with lactic acid bacteria isolated from Kimchi in high-fat diet-induced obese rats.

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پیوند در کلیپ بورد ذخیره می شود
Na-Hyung Kim
Phil-Dong Moon
Su-Jin Kim
In-Young Choi
Hyo-Jin An
Noh-Yil Myung
Hyun-Ja Jeong
Jae-Young Um
Seung-Heon Hong
Hyung-Min Kim

کلید واژه ها

خلاصه

Lactic acid bacteria are known to exert various physiologic functions in humans. In the current study, we investigated the effects of Soypro, a new soymilk fermented with lactic acid bacteria, like Leuconostoc kimchii, Leuconostoc citreum, and Lactobacillus plantarum, isolated from Kimchi, on adipocyte differentiation in preadipocyte 3T3-L1 cell lines and weight gain or the plasma lipid profile in Sprague-Dawley rats. Adipocyte 3T3-L1 cells treated with Soypro (10 microg/ml) significantly reduced the contents of cellular triglyceride and inhibited cell differentiation by Oil red O staining. Treatment with Soypro (10 microg/ml) for an additional two days in adipocytes inhibited the expression of peroxisome proliferator-activated receptor-gamma2 and CCAAT/enhancer binding protein-alpha, transcription factors of adipocyte differentiation. Based on these in vitro studies, we examined the anti-obesity effect of Soypro in rats for six weeks. Soypro had no significant effect on high-fat diet-induced increases in body weight, food intake, or feed gain ratio. However, the administration of Soypro significantly reduced the concentration of the plasma low density lipoprotein cholesterol. Changes in the plasma levels of total cholesterol and glucose were inclined to decrease in Soypro administrated groups compared with saline treated group. Triglyceride and high density lipoprotein cholesterol values in Soypro fed groups were similar compared to those of saline fed groups. Although further research is needed, these findings suggest that Soypro decreased the levels of low density lipoprotein cholesterol in high-fat diet-induced obesity and might partially inhibit the adipocyte differentiation through the suppression of a transcription factors peroxisome proliferator-activated receptor-gamma2 and CCAAT/enhancer binding protein-alpha.

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