Effects of Korean Red Ginseng extract on hepatic lipid accumulation in HepG2 cells

Lee, Mak-Soon; Kim, Chong Tai; Kim, In Hwan; Kim, Yangha

doi:10.1080/09168451.2014.997186

Cited by 8 publications

(6 citation statements)

References 25 publications

(18 reference statements)

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“…Numerous in vitro research reports have documented that ginseng and ginsenosides can activate the AMPK pathway resulting in increased levels of p-AMPK and phospho-acetyl-CoA carboxylase in hepatocyte HepG2 cells [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] ( Table 1 ). By activating this pathway, ginseng and ginsenosides can, in vitro , suppress the expression of fatty acid synthase (FAS), 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR), phosphoenolpyruvate carboxykinase (PEPCK), and glucose 6-phosphatase (G6Pase)—thereby inhibiting TAG synthesis [27] , [28] , [31] , cholesterogenesis [28] , [33] , and gluconeogenesis [29] , [30] , [34] .…”

Section: Effect On Livermentioning

confidence: 99%

Ginseng and obesity

2018

Journal of Ginseng Research

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Although ginseng has been shown to have an antiobesity effect, antiobesity-related mechanisms are complex and have not been completely elucidated. In the present study, we evaluated ginseng’s effects on food intake, the digestion, and absorption systems, as well as liver, adipose tissue, and skeletal muscle in order to identify the mechanisms involved. A review of previous in vitro and in vivo studies revealed that ginseng and ginsenosides can increase energy expenditure by stimulating the adenosine monophosphate-activated kinase pathway and can reduce energy intake. Moreover, in high fat diet-induced obese and diabetic individuals, ginseng has shown a two-way adjustment effect on adipogenesis. Nevertheless, most of the previous studies into antiobesity effects of ginseng have been animal based, and there is a paucity of evidence supporting the suggestion that ginseng can exert an antiobesity effect in humans.

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Section: Effect On Livermentioning

confidence: 99%

Ginseng and obesity

2018

Journal of Ginseng Research

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“…Alcoholic fatty liver is a uniform response by the liver toward alcohol that can progress, resulting in increasingly severe liver diseases. Despite the growing body of literature on the functionality of KRG [19,20], the preventive effects of ginseng against alcohol-induced fatty liver in vivo and the underlying mechanism responsible for it remain unclear. Therefore, in the present study, we tested the hypothesis that KRG has a preventive effect against alcoholic fatty liver, focusing on the role of lipid metabolic homeostasis at the liver-adipose tissue axis.…”

Section: Resultsmentioning

confidence: 99%

Protective Effects of Korean Red Ginseng against Alcohol-Induced Fatty Liver in Rats

Ok¹,

Kwon²

2015

Molecules

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The present study tested the hypothesis that Korean red ginseng (KRG) provides a protective effect against alcoholic fatty liver. Male Sprague-Dawley rats were divided into four groups and fed a modified Lieber-DeCarli diet containing 5% (w/v) alcohol or an isocaloric amount of dextrin-maltose for the controls for 6 weeks: normal control (CON), alcohol control (ET), and ET treated with 125 or 250 mg/kg body weight/day of KRG (RGL or RGH, respectively). Compared with the CON group, the ET group exhibited a significant increase in triglycerides, total cholesterol and the presence of lipid droplets in the liver, and a decrease in fat mass, which were all attenuated by KRG supplementation in adose-dependent manner. The mitigation was accompanied by AMP-activated protein kinase (AMPK) signaling pathways in the liver and adipose tissue. In addition, suppression in the alcohol-induced changes of adipose adipokine mRNA expression was also observed in KRG supplementation group. These findings suggest that KRG may have the potential to ameliorate alcoholic fatty liver by suppressing inappropriate lysis of adipose tissue and preventing unnecessary de novo lipogenesis in the liver, which are mediated by AMPK signaling pathways. A mechanism for an interplay between the two organs is still needed to be examined with further assays.

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“…showed that ginsenoside Rb1 regulates appetite and achieves energy balance by modulating the expression of inflammatory factors in vivo and restoring the anorexigenic effects of leptin and leptin p-STAT3 Frontiers in Pharmacology frontiersin.org signaling in the hypothalamus in mice fed a high-fat diet. In vitro studies have shown that ginsenosides can inhibit triglyceride synthesis, cholesterol production (Lee et al, 2015), gluconeogenesis (Quan et al, 2012) by activating AMPK and inhibiting fatty acid synthase (FAS) and 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMGCR). Ginseng reduced adipocyte size and fat storage in highfat diet-induced obese mice and rats (Lee et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

(20R)-panaxadiol improves obesity by promoting white fat beigeing

Lv²,

Feng³

et al. 2023

Front. Pharmacol.

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Introduction: Obesity is an important cause of a range of metabolic diseases. However, the complex mechanisms of obesity and its related diseases make some weight loss methods ineffective or have safety issues. Ginseng, a specialty of Jilin Province in China with both edible and medicinal value, contains mainly ginsenosides and other components. In order to study the anti-obesity effect of ginseng, network pharmacology was used to predict and screen the active ingredients, action targets and signaling pathways of ginseng. We found (20R)-panaxadiol (PD) is a more desirable active ingredient due to its high drug-like properties and high bioavailability. Moreover, it is closely related to cAMP pathway which is more important in metabolism regulation. The corresponding pharmacodynamic targets of PD include ADRB2 (the gene encoding the β2-adrenoceptor receptor). Our study aimed to investigate whether Panaxadiol can promote white adipocyte beigeing and increase thermogenesis through modulating the β2/cAMP pathway to exert anti-obesity effects.Methods:In vivo, we established high-fat feeding obesity model, genotypically obese mice (ob/ob) model, and administered PD (10 mg/kg). PD treatment in ob/ob mice along with β2 receptor inhibitor ICI118551. In vitro, differentiated mature 3T3-L1 cells were given palmitate (PA) to induce hypertrophy model along with PD (20 μM).Results: The results of this study demonstrated that PD significantly reduced body weight, improved glucose tolerance and lipid levels in high-fat-induced obese mice and ob/ob mice, and also reduced lipid droplet size in PA-treated hypertrophic adipocytes in vitro. Molecular biology assays confirmed that cAMP response element binding protein (CREB) phosphorylation was increased after PD administration, and the expression of thermogenesis-related proteins UCP1, PRDM16 and mitochondrial biosynthesis-related proteins PGC-1α, TFAM and NRF1 were increased. Molecular docking results showed a low binding energy between β2 receptors and PD, indicating an affinity between the β2 receptor and PD. In addition, the β2 receptor inhibition, reversed the anti-obesity effect of PD on the body weight, lipid droplets, the expression of thermogenesis-related proteins and CREB phosphorylation in ob/ob mice.Discussion: These results suggest that PD may promote the expression of thermogenic proteins through phosphorylation of CREB via β2 receptor activation, and thus exert anti-obesity effects.

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Effects of Korean Red Ginseng extract on hepatic lipid accumulation in HepG2 cells

Cited by 8 publications

References 25 publications

Ginseng and obesity

Ginseng and obesity

Protective Effects of Korean Red Ginseng against Alcohol-Induced Fatty Liver in Rats

(20R)-panaxadiol improves obesity by promoting white fat beigeing

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