American Ginseng Stimulates Insulin Production and Prevents Apoptosis through Regulation of Uncoupling Protein‐2 in Cultured β Cells

Luo, John Zq; Luo, Liqiang

doi:10.1093/ecam/nel026

Cited by 61 publications

(55 citation statements)

References 39 publications

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“…Therefore, reduction or regulation of UCP-2 levels by GA, increased ATP levels and enhanced insulin secretion observed in our study in RINm5F cells is an important observation. Consistent with our study, Luo and Luo (2006) have demonstrated that American Ginseng stimulates insulin production and prevents apoptosis through the regulation of UCP-2 in cultured β-cells.…”

Section: Discussionsupporting

confidence: 93%

Gallic acid protects RINm5F β‐cells from glucolipotoxicity by its antiapoptotic and insulin‐secretagogue actions

Sameermahmood

Raji

Thangavel

et al. 2010

Phytotherapy Research

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Gallic acid is claimed to possess antioxidant, antiinflammatory and cytoprotective effects. Since pancreatic islets from Type 2 diabetic patients have functional defects, it was hypothesized that glucolipotoxicity might induce apoptosis in beta-cells and gallic acid could offer protection. To test this, RINm5F beta-cells were exposed to high glucose (25 microM) or palmitate (500 microM) or a combination of both for 24 h in the presence and absence of gallic acid. Cells subjected to glucolipotoxicity in the absence and presence of gallic acid were assessed for DNA damage by comet assay. Apoptosis was inferred by caspase-3 protein expression and caspase-3 activity and changes in Bcl-2 mRNA. RT-PCR was used to analyse PDX-1, insulin and UCP-2 mRNA expression in RINm5F beta-cells and insulin levels were quantified from the cell culture supernatant. NFkappaB signal was studied by EMSA, immunofluorescence and Western blot analysis. While RINm5F beta-cells subjected to glucolipotoxicity exhibited increased DNA damage, apoptotic markers and NFkappaB signals, all these apoptotic perturbations were resisted by gallic acid. Gallic acid dose-dependently increased insulin secretion in RINm5F beta-cells and upregulated mRNA of PDX-1 and insulin. It is suggested that the insulin-secretagogue and transcriptional regulatory action of gallic acid is a newly identified mechanism in our study.

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Section: Discussionsupporting

confidence: 93%

Gallic acid protects RINm5F β‐cells from glucolipotoxicity by its antiapoptotic and insulin‐secretagogue actions

Sameermahmood

Raji

Thangavel

et al. 2010

Phytotherapy Research

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“…This mechanism is related to release of neurotransmitter acetylcholine from nerve terminals in pancreases and stimulation of muscarinic M (3) receptors in β-cells (40;43). Finally, ginseng may prevent β-cell apoptosis (44). This mechanism is related to inhibition of uncoupling protein 2 (UCP2) expression in mitochondria, and an increase in ATP production.…”

Section: Ginseng On β Cellsmentioning

confidence: 99%

Traditional Chinese Medicine in Treatment of Metabolic Syndrome

Yin¹,

Zhang²,

Ye³

2008

EMIDDT

338

220

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In management of metabolic syndrome, the traditional Chinese medicine (TCM) is an excellent representative in alternative and complementary medicines with a complete theory system and substantial herb remedies. In this article, basic principle of TCM is introduced and 22 traditional Chinese herbs are reviewed for their potential activities in the treatment of metabolic syndrome. Three herbs, ginseng, rhizoma coptidis (berberine, the major active compound) and bitter melon, were discussed in detail on their therapeutic potentials. Ginseng extracts made from root, rootlet, berry and leaf of Panax quinquefolium (American ginseng) and Panax ginseng (Asian ginseng), are proved for anti-hyperglycemia, insulin sensitization, islet protection, anti-obesity and anti-oxidation in many model systems. Energy expenditure is enhanced by ginseng through thermogenesis. Ginseng-specific saponins (ginsenosides) are considered as the major bioactive compounds for the metabolic activities of ginseng. Berberine from rhizoma coptidis is an oral hypoglycemic agent. It also has anti-obesity and anti-dyslipidemia activities. The action mechanism is related to inhibition of mitochondrial function, stimulation of glycolysis, activation of AMPK pathway, suppression of adipogenesis and induction of low-density lipoprotein (LDL) receptor expression. Bitter melon or bitter gourd (Momordica charantia) is able to reduce blood glucose and lipids in both normal and diabetic animals. It may also protect β cells, enhance insulin sensitivity and reduce oxidative stress. Although evidence from animals and humans consistently supports the therapeutic activities of ginseng, berberine and bitter melon, multi-center large-scale clinical trials have not been conducted to evaluate the efficacy and safety of these herbal medicines.Metabolic syndrome characterized by insulin resistance has become a health thread worldwide in the past 20 years (1). In survey of 8,814 people in USA, prevalence of metabolic syndrome was over 40% in people of 60-69 year old (2). In the other geographic areas in the world including Europe and Asia, the prevalence of metabolic syndrome has been increasing dramatically (1). Metabolic syndrome and associated diseases have been one of major burdens in health care system in many industrialized countries.The concept of metabolic syndrome was generated by Kylin in 1923, who described a cluster of medical conditions, such as hypertension, hyperglycemia and gout (3). The concept did not attract much attention until Dr. Gerald Reaven introduced the syndrome X in 1988 (4), which is similar to the metabolic syndrome. In 1999, WHO (World Health Organization) and EGIR (European Group for the Study of Insulin Resistance) released their diagnostic criteria for the metabolic syndrome, respectively (5;6). Now, there are at least 6 sets of diagnostic criteria for the syndrome from different organizations over the world (1;7). The primary contents of diagnostic criteria are similar among these organizations. They are hyperglycemia, insulin r...

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“…Some studies have demonstrated that ginseng may enhance glucosestimulated insulin secretion via increasing ATP levels, affecting activity of K ATP channels and Ca 2C channels (Luo & Luo 2006, Park et al 2008a. We discovered that Rb1 significantly increased the ATP:ADP ratio and cytosolic Ca 2C levels in NCI-H716 cells.…”

Section: Discussionmentioning

confidence: 71%

Increased glucagon-like peptide-1 secretion may be involved in antidiabetic effects of ginsenosides

Liu

Zhang

et al. 2013

Journal of Endocrinology

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Panax ginseng is one of the most popular herbal remedies. Ginsenosides, major bioactive constituents in P. ginseng, have shown good antidiabetic action, but the precise mechanism was not fully understood. Glucagon-like peptide-1 (GLP1) is considered to be an important incretin that can regulate glucose homeostasis in the gastrointestinal tract after meals. The aim of this study was to investigate whether ginseng total saponins (GTS) exerts its antidiabetic effects via modulating GLP1 release. Ginsenoside Rb1 (Rb1), the most abundant constituent in GTS, was selected to further explore the underlying mechanisms in cultured NCI-H716 cells. Diabetic rats were developed by a combination of high-fat diet and low-dose streptozotocin injection. The diabetic rats orally received GTS (150 or 300 mg/kg) daily for 4 weeks. It was found that GTS treatment significantly ameliorated hyperglycemia and dyslipidemia, accompanied by a significant increase in glucose-induced GLP1 secretion and upregulation of proglucagon gene expression. Data from NCI-H716 cells showed that both GTS and Rb1 promoted GLP1 secretion. It was observed that Rb1 increased the ratio of intracellular ATP to ADP concentration and intracellular Ca 2C concentration. The metabolic inhibitor azide (3 mM), the K ATP channel opener diazoxide (340 mM), and the Ca 2C channel blocker nifedipine (20 mM) significantly reversed Rb1-mediated GLP1 secretion. All these results drew a conclusion that ginsenosides stimulated GLP1 secretion both in vivo and in vitro. The antidiabetic effects of ginsenosides may be a result of enhanced GLP1 secretion. Key Words" glucagon-like peptide-1 (GLP1)" ginsenosides " Rb1" type 2 diabetes " ginseng total saponins (GTS)

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American Ginseng Stimulates Insulin Production and Prevents Apoptosis through Regulation of Uncoupling Protein‐2 in Cultured β Cells

Cited by 61 publications

References 39 publications

Gallic acid protects RINm5F β‐cells from glucolipotoxicity by its antiapoptotic and insulin‐secretagogue actions

Gallic acid protects RINm5F β‐cells from glucolipotoxicity by its antiapoptotic and insulin‐secretagogue actions

Traditional Chinese Medicine in Treatment of Metabolic Syndrome

Increased glucagon-like peptide-1 secretion may be involved in antidiabetic effects of ginsenosides

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