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Metformin as an oral glucose-lowering drug is used to treat type 2 diabetic mellitus. Considering the relatively high incidence of cardiovascular complications and other metabolic diseases in diabetic mellitus patients, a combination of metformin plus herbal supplements is a preferrable way to improve the therapeutic outcomes of metformin. Ginseng berry, the fruit of Panax ginseng Meyer, has investigated as a candidate in metformin combination mainly due to its anti-hyperglycemic, anti-hyperlipidemic, antiobesity, anti-hepatic steatosis and anti-inflammatory effects. Moreover, the pharmacokinetic interaction of metformin via OCTs and MATEs leads to changes in the efficacy and/or toxicity of metformin. Thus, we assessed how ginseng berry extract (GB) affects metformin pharmacokinetics in mice, specially focusing on the effect of the treatment period (i.e., 1-day and 28-day) of GB on metformin pharmacokinetics. In 1-day and 28-day co-treatment of metformin and GB, GB did not affect renal excretion as a main elimination route of metformin and GB therefore did not change the systemic exposure of metformin. Interestingly, 28-day co-treatment of GB increased metformin concentration in the livers (i.e., 37.3, 59.3% and 60.9% increases versus 1-day metformin, 1-day metformin plus GB and 28-day metformin groups, respectively). This was probably due to the increased metformin uptake via OCT1 and decreased metformin biliary excretion via MATE1 in the livers. These results suggest that co-treatment of GB for 28 days (i.e., long-term combined treatment of GB) enhanced metformin concentration in the liver as a pharmacological target tissue of metformin. However, GB showed a negligible impact on the systemic exposure of metformin in relation to its toxicity (i.e., renal and plasma concentrations of metformin). [ABSTRACT FROM AUTHOR]

Ginseng berry extract contains plenty of ginsenosides showing anti-obesity and anti-hyperglycemic activities. Regarding that long-term intakes of herbal products to control metabolic disorders as popular alternatives have become popular, ginseng berry extract plus metformin is an attractive item for long-term glycemic control. Herein, we investigated the effect of ginseng berry extract (GBE) or its combination with metformin against obesity and hepatic steatosis in high-fat diet fed mice.GBE altered abnormal features (e.g. body weight, serum profiles, hepatic steatosis/inflammation and fat mass). Concomitantly, GBE increased mRNA levels of adiponectin and CCAAT/enhancer binding protein. All these changes were observed in metformin alone and GBE plus metformin. Moreover, in GBE plus metformin intake, GBE increased organic cation transporter-mediated metformin uptake in liver and mRNA of AMP-activated protein kinase together, which additively ameliorated obesity and hepatic steatosis. Therefore, GBE itself and GBE plus metformin could be useful to regulate metabolic disorders.

In GBE plus metformin treatment, GBE plus metformin showed the additive efficacy against obesity, hepatic steatosis and hyperglycemia! • GBE ameliorated obesity and hepatic steatosis in mice fed high-fat diet. • GBE increased organic cation transporter-mediated metformin uptake in liver. • GBE plus metformin additively ameliorated obesity and hepatic steatosis. • GBE itself and GBE plus metformin could be useful to regulate metabolic disorders. Ginseng berry extract contains plenty of ginsenosides showing anti-obesity and anti-hyperglycemic activities. Regarding that long-term intakes of herbal products to control metabolic disorders as popular alternatives have become popular, ginseng berry extract plus metformin is an attractive item for long-term glycemic control. Herein, we investigated the effect of ginseng berry extract (GBE) or its combination with metformin against obesity and hepatic steatosis in high-fat diet fed mice. GBE altered abnormal features (e.g. body weight, serum profiles, hepatic steatosis/inflammation and fat mass). Concomitantly, GBE increased mRNA levels of adiponectin and CCAAT/enhancer binding protein. All these changes were observed in metformin alone and GBE plus metformin. Moreover, in GBE plus metformin intake, GBE increased organic cation transporter-mediated metformin uptake in liver and mRNA of AMP-activated protein kinase together, which additively ameliorated obesity and hepatic steatosis. Therefore, GBE itself and GBE plus metformin could be useful to regulate metabolic disorders. [ABSTRACT FROM AUTHOR]