Kastre edilmiş yüksek yağlı diyetle beslenen ratlarda panax in obesite inhibisyonu ve düzelmiş lipit metobolizması üzerine etkisi.
Korean red ginseng (Panax ginseng) inhibits obesity and improves lipid metabolism in high fat diet-fed castrated mice.
Shin S S, Yoon M.
Abstract
Ethnopharmacological Relevance:
Korean red ginseng (Panax ginseng C.A. Meyer, Araliaceae) has been historically used as a traditional drug for the prevention and treatment of most ageing-related diseases, such as obesity, dyslipidemia, diabetes, and cardiovascular disease. Elderly men with testosterone deficiency are strongly associated with many of the aforementioned metabolic diseases. The aim of this study was to determine the effects of ginseng on obesity and lipid metabolism in a mouse model of testosterone deficiency (castrated C57BL/6J mice).
Materials And Methods:
The effects of ginseng extract (GE) on obesity and lipid metabolism in high-fat diet (HFD)-fed castrated C57BL/6J mice were examined using hematoxylin and eosin staining, serum lipid analysis, and quantitative real-time polymerase chain reaction (PCR). The effects of GE, ginsenosides, and testosterone on adipogenesis were measured using Oil Red O staining, XTT assay, and real-time PCR.
Results:
Compared with HFD mice, mice receiving HFD supplemented with GE (HFD-GE) for 8 weeks showed decreased body weight, adipose tissue mass, and adipocyte size without affecting food intake. Serum levels of triglycerides and total cholesterol were lowered in HFD-GE mice than in HFD mice. GE also markedly reduced HFD-induced hepatic lipid accumulation. Concomitantly, HFD-GE decreased mRNA expression of adipogenesis-related genes (SREBP-1C, PPARγ, FAS, SCD1, and ACC1) in visceral adipose tissues compared with HFD alone. Consistent with the in vivo data, GE and major active ginsenosides (Rb1 and Rg1) decreased lipid accumulation and mRNA expression of PPARγ, C/EBPα, and SCD1 in 3T3-L1 adipocytes compared with control. Similarly, testosterone also decreased lipid accumulation and mRNA levels of PPARγ, C/EBPα, and SCD1. These inhibitory effects were further increased by co-treatment of GE or ginsenosides with testosterone.
Conslusions:
Our results demonstrate that ginseng can inhibit obesity and dyslipidemia in HFD-fed castrated mice, possibly by inhibiting adipogenic gene expression. In addition, our results indicate that ginseng may act like testosterone to inhibit adipogenesis, suggesting that ginseng may be able to prevent obesity, hyperlipidemia, and hepatic steatosis in men with testosterone deficiency.
