Rho , a Fraction From Rhodiola crenulate , Ameliorates Hepatic Steatosis in Mice Models

• Published in: Frontiers in physiology 2018-03, Vol.9, p.222-222
• Main Authors: Yi, Qin, Sun, Puyang, Li, Juan, Kong, Siming, Tian, Jinying, Li, Xuechen, Yang, Yanan, Zhang, Peicheng, Liu, Yuying, Han, Jingyan, Zhang, Xiaolin, Ye, Fei
• Format: Article
• Language: English
• Subjects: a fraction from Rhodiola crenulate (Rho); hepatic lipid metabolism; hepatic steatosis; insulin resistance; non-alcoholic fatty liver disease (NAFLD); Physiology
• ISSN: 1664-042X; 1664-042X
• DOI: 10.3389/fphys.2018.00222

The prevalence of non-alcoholic fatty liver disease (NAFLD), which is developed from hepatic steatosis, is increasing worldwide. However, no specific drugs for NAFLD have been approved yet. To observe the effects of , a fraction from , on non-alcoholic hepatic steatosis, three mouse models with characteristics of NAFLD were used including high-fat diet (HFD)-induced obesity (DIO) mice, KKAy mice, and HFD combined with tetracycline stimulated Model-T mice. Hepatic lipid accumulation was determined via histopathological analysis and/or hepatic TG determination. The responses to insulin were evaluated by insulin tolerance test (ITT), glucose tolerance test (GTT), and hyperinsulinemic-euglycemic clamp, respectively. The pathways involved in hepatic lipid metabolism were observed via western-blot. Furthermore, the liver microcirculation was observed by inverted microscopy. The HPLC analysis indicated that the main components of were flavan polymers. The results of histopathological analysis showed that could ameliorate hepatic steatosis in DIO, KKAy, and Model-T hepatic steatosis mouse models, respectively. After treatment in DIO mice, insulin resistance was improved with increasing glucose infusion rate (GIR) in hyperinsulinemic-euglycemic clamp, and decreasing areas under the blood glucose-time curve (AUC) in both ITT and GTT; the pathways involved in fatty acid uptake and lipogenesis were both down-regulated, respectively. However, the pathways involved in beta-oxidation and VLDL-export on hepatic steatosis were not changed significantly. The liver microcirculation disturbances were also improved by in DIO mice. These results suggest that is a lead nature product for hepatic steatosis treatment. The mechanism is related to enhancing insulin sensitivity, suppressing fatty acid uptake and inhibiting lipogenesis in liver.