Search

This study investigated the effects of ginseng berry extract (GBE) and its major ginsenoside Re (GinRe) on skeletal muscle atrophy and exercise performance. GBE and GinRe upregulated the mRNA expression of sirtuin1 (Sirt1) and peroxisome proliferator-activated receptor-γ coactivator-1α (Pgc-1α) in C2C12 myotubes. Administration of GBE and GinRe in high-fat diet-induced muscle atrophy mice enhanced endurance exercise performance and increased skeletal muscle weight with a significant downregulation of skeletal muscle atrophy genes and upregulation of oxidative myosin heavy chain subtypes, mitochondrial biogenesis, and oxidative phosphorylation regulatory genes in skeletal muscle tissue. Oral administration of GBE and GinRe enhanced the protein expression of SIRT1, phosphorylation of adenosine monophosphate-activated protein kinase (AMPK)/PGC-1α/peroxisome proliferator-activated receptor-δ (PPARδ) signaling axis in skeletal muscle tissue, acting as an exercise metabolism regulator. These results suggest that GBE and GinRe have the potential to enhance exercise performance through mitochondrial biogenesis.

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]

Sarcopenia and obesity are serious health problems that are highly related to several metabolic diseases. Sarcopenic obesity, a combined state of sarcopenia and obesity, results in higher risks of metabolic diseases and even mortality than sarcopenia or obesity alone. Therefore, the development of therapeutic agents for sarcopenic obesity is crucial. C57BL/6 mice were fed with a high-fat diet (HFD) for 9 weeks. Then, mice were administered with Panax ginseng berry extract (GBE) for an additional 4 weeks, with continuous HFD intake. GBE significantly decreased the food efficiency ratio, serum lipid and insulin levels, adipose tissue weights, and adipocyte size. It significantly increased the grip strength, muscle masses, and myofiber cross-sectional area. It deactivated the protein kinase C (PKC) theta and zeta, resulting in activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway, which is known to regulate muscle synthesis and degradation. Furthermore, it inhibited the production of inflammatory cytokines in the muscle tissue. GBE attenuated both obesity and sarcopenia. Thus, GBE is a potential agent to prevent or treat sarcopenic obesity. [ABSTRACT FROM AUTHOR]

[Display omitted] • GBE and ginsenoside Re reduced body weight gain in high-fat diet-fed mice. • GBE and ginsenoside Re induced favorable changes in blood lipid levels and glucose. • GBE and ginsenoside Re improved exercise performance and muscle mass. • GBE and ginsenoside Re activated Sirt1/AMPK/PGC-1α/PPARδ signaling pathway and promoted mitochondrial biogenesis. This study investigated the effects of ginseng berry extract (GBE) and its major ginsenoside Re (GinRe) on skeletal muscle atrophy and exercise performance. GBE and GinRe upregulated the mRNA expression of sirtuin1 (Sirt1) and peroxisome proliferator-activated receptor-γ coactivator-1α (Pgc-1α) in C2C12 myotubes. Administration of GBE and GinRe in high-fat diet-induced muscle atrophy mice enhanced endurance exercise performance and increased skeletal muscle weight with a significant downregulation of skeletal muscle atrophy genes and upregulation of oxidative myosin heavy chain subtypes, mitochondrial biogenesis, and oxidative phosphorylation regulatory genes in skeletal muscle tissue. Oral administration of GBE and GinRe enhanced the protein expression of SIRT1, phosphorylation of adenosine monophosphate-activated protein kinase (AMPK)/PGC-1α/peroxisome proliferator-activated receptor-δ (PPARδ) signaling axis in skeletal muscle tissue, acting as an exercise metabolism regulator. These results suggest that GBE and GinRe have the potential to enhance exercise performance through mitochondrial biogenesis. [ABSTRACT FROM AUTHOR]

Sarcopenia and obesity are serious health problems that are highly related to several metabolic diseases. Sarcopenic obesity, a combined state of sarcopenia and obesity, results in higher risks of metabolic diseases and even mortality than sarcopenia or obesity alone. Therefore, the development of therapeutic agents for sarcopenic obesity is crucial. C57BL/6 mice were fed with a high-fat diet (HFD) for 9 weeks. Then, mice were administered with Panax ginseng berry extract (GBE) for an additional 4 weeks, with continuous HFD intake. GBE significantly decreased the food efficiency ratio, serum lipid and insulin levels, adipose tissue weights, and adipocyte size. It significantly increased the grip strength, muscle masses, and myofiber cross-sectional area. It deactivated the protein kinase C (PKC) theta and zeta, resulting in activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway, which is known to regulate muscle synthesis and degradation. Furthermore, it inhibited the production of inflammatory cytokines in the muscle tissue. GBE attenuated both obesity and sarcopenia. Thus, GBE is a potential agent to prevent or treat sarcopenic obesity.

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, anti-obesity, 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)., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Lee, You, Yim, Han, Chae, Bae, Kim, Yu, Jung, Nhoek, Kim, Choi, Chin, Kim and Choi.)