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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.

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.

The role of ginseng berry extract (GBE) has been attributed to its anti-hyperglycemic effect in humans. However, the pharmacokinetic characteristics of GBE constitutes after oral GBE administration have not been established yet. In this study, stereoselective and simultaneous analytical methods for 10 ginsenosides (ginsenoside Rb1, Rb2, Rc, Rd, Re, Rg1, S-Rg2, R-Rg2, S-Rg3, and R-Rg3) were developed using ultra-performance liquid chromatography, coupled with electrospray ionization triple quadrupole tandem mass spectrometry (UPLC-MS/MS), for the pharmacokinetic study of GBE. Furthermore, the pharmacokinetic profiles of 10 ginsenosides after oral GBE were evaluated in rats. All analytes were detected with a linear concentration range of 0.01–10 µg/mL. Lower limits of detection (LLOD) and quantification (LLOQ) were 0.003 and 0.01 µg/mL, respectively, for all 10 ginsenosides. This established method was adequately validated in linearity, sensitivity, intra- and inter-day precision, accuracy, recovery, matrix effect, and stability. Relative standard deviations for all intra- and inter-precision of the 10 ginsenosides were below 11.5% and accuracies were 85.3–111%, which were sufficient to evaluate the pharmacokinetic study of oral GBE in rats. We propose that Rb1, Rb2, Rc, Rd, Re, Rg1, S-Rg2, R-Rg2 and/or S-Rg3 were appropriate pharmacokinetic markers of systemic exposure following oral GBE administration.

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.)

This study investigates the in vivo functions of ginseng berry extract (GB) as a therapy for dextran sodium sulfate (DSS)-induced colitis. C57BL/6 mice were given drinking water containing DSS (3%) for eight days to induce acute colitis. At the same time, the mice received an oral dose of GB (50 mg/kg) once daily. The GB-treated mice were less susceptible to the development of acute colitis than were control mice treated with saline, as determined by weight loss, disease activity, and colon histology. The administration of GB to DSS-treated mice also reduced the numbers and inhibited the activation of colon-infiltrating T cells, neutrophils, intestinal CD103-CD11c+ dendritic cells (cDCs), and macrophages. In addition, GB treatment promoted the migration of CD103+CD11c+ cDCs and expansion of Foxp3+ regulatory T cells in the colons of DSS-treated mice. Similarly, in the DSS-induced chronic colitis model, GB treatment improved the macroscopic and histological appearance of the colon wall when compared to untreated control mice, as indicated by longer colon length and lower histological scores. This is the first report to show that oral administration of GB suppresses immune activation and protects against experimentally induced colitis. [ABSTRACT FROM AUTHOR]

The role of ginseng berry extract (GBE) has been attributed to its anti-hyperglycemic effect in humans. However, the pharmacokinetic characteristics of GBE constitutes after oral GBE administration have not been established yet. In this study, stereoselective and simultaneous analytical methods for 10 ginsenosides (ginsenoside Rb1, Rb2, Rc, Rd, Re, Rg1, S-Rg2, R-Rg2, S-Rg3, and R-Rg3) were developed using ultra-performance liquid chromatography, coupled with electrospray ionization triple quadrupole tandem mass spectrometry (UPLC-MS/MS), for the pharmacokinetic study of GBE. Furthermore, the pharmacokinetic profiles of 10 ginsenosides after oral GBE were evaluated in rats. All analytes were detected with a linear concentration range of 0.01–10 µg/mL. Lower limits of detection (LLOD) and quantification (LLOQ) were 0.003 and 0.01 µg/mL, respectively, for all 10 ginsenosides. This established method was adequately validated in linearity, sensitivity, intra- and inter-day precision, accuracy, recovery, matrix effect, and stability. Relative standard deviations for all intra- and inter-precision of the 10 ginsenosides were below 11.5% and accuracies were 85.3–111%, which were sufficient to evaluate the pharmacokinetic study of oral GBE in rats. We propose that Rb1, Rb2, Rc, Rd, Re, Rg1, S-Rg2, R-Rg2 and/or S-Rg3 were appropriate pharmacokinetic markers of systemic exposure following oral GBE administration. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study was to determine whether ginseng berry extract improves blood circulation by regulating vasodilator expression in exposed to tumor necrosis factor alpha (TNF-α)-exposed endothelial cells and muscle cells., Methods: Nitric oxide (NO) and cGMP levels in human umbilical vein endothelial cells (HUVECs) and A7r5 cells exposed to ginseng berry extract were investigated. Based on the in vitro results, healthy participants were treated with ginseng berry extract for 4 weeks and then a non-invasive vascular screening device was used to confirm the improvement of blood circulation., Results: When TNF-α-treated cells were exposed to the ginseng berry extract, the expression levels of endothelial nitric oxide synthase (eNOS), NO, and cGMP were recovered to almost normal levels. In addition, TNF-ɑ-induced overexpression of vascular cell adhesion molecule 1 (VCAM-1), intracellular adhesion molecule 1 (ICAM-1), e-selectin, and p-selectin was lowered by ginseng berry extract. The ginseng berry extract significantly increased ankle brachial pressure index compared to placebo (p < 0.05)., Conclusion: This study confirmed that the intake of ginseng berry extract improved blood circulation and therefore, its intake would be helpful for people having problems with blood circulation., (©2018 The Korean Society for Exercise Nutrition.)

This study investigates the in vivo functions of ginseng berry extract (GB) as a therapy for dextran sodium sulfate (DSS)-induced colitis. C57BL/6 mice were given drinking water containing DSS (3%) for eight days to induce acute colitis. At the same time, the mice received an oral dose of GB (50 mg/kg) once daily. The GB-treated mice were less susceptible to the development of acute colitis than were control mice treated with saline, as determined by weight loss, disease activity, and colon histology. The administration of GB to DSS-treated mice also reduced the numbers and inhibited the activation of colon-infiltrating T cells, neutrophils, intestinal CD103(-)CD11c⁺ dendritic cells (cDCs), and macrophages. In addition, GB treatment promoted the migration of CD103⁺CD11c⁺ cDCs and expansion of Foxp3⁺ regulatory T cells in the colons of DSS-treated mice. Similarly, in the DSS-induced chronic colitis model, GB treatment improved the macroscopic and histological appearance of the colon wall when compared to untreated control mice, as indicated by longer colon length and lower histological scores. This is the first report to show that oral administration of GB suppresses immune activation and protects against experimentally induced colitis.