Beneficial effects of IH-901 on glucose and lipid metabolisms via activating adenosine monophosphate-activated protein kinase and phosphatidylinositol-3 kinase pathways.

@article{Yuan2011BeneficialEO,
  title={Beneficial effects of IH-901 on glucose and lipid metabolisms via activating adenosine monophosphate-activated protein kinase and phosphatidylinositol-3 kinase pathways.},
  author={Hai-Dan Yuan and Sung Jip Kim and Sung Hyun Chung},
  journal={Metabolism: clinical and experimental},
  year={2011},
  volume={60 1},
  pages={
          43-51
        }
}
View on PubMed
metabolictrial.com
24 Citations
Background Citations
7

Figures and Tables from this paper

24 Citations

Citation Type

Citation Type

Ginsenoside Re lowers blood glucose and lipid levels via activation of AMP-activated protein kinase in HepG2 cells and high-fat diet fed mice.
TLDR
It is suggested that ginsenoside Re improves hyperglycemia and hyperlipidemia through activation of AMPK, and confers beneficial effects on type 2 diabetic patients with insulin resistance and dyslipidia.
Inhibition of Cholesterol Synthesis in HepG2 Cells by GINST-Decreasing HMG-CoA Reductase Expression Via AMP-Activated Protein Kinase.
TLDR
GINST inhibits cholesterol synthesis in HepG2 cells by decreasing HMGCR expression via AMPKα activation, and it is suggested that GINST can be used to reduce hypercholesterolemia.
Ginsenoside Rg2 induces orphan nuclear receptor SHP gene expression and inactivates GSK3β via AMP-activated protein kinase to inhibit hepatic glucose production in HepG2 cells.
Ginsenoside metabolite compound K stimulates glucagon-like peptide-1 secretion in NCI-H716 cells via bile acid receptor activation
TLDR
The data provide a novel mechanism of CK for antidiabetic effects and might suggest that CK is a potential agent that has multiple biological functions in the body via GLP-1 secretion and TGR5 activation.
AMP-activated protein kinase: An emerging target for ginseng
Ginseng metabolite Protopanaxadiol induces Sestrin2 expression and AMPK activation through GCN2 and PERK
TLDR
The results suggest that ginseng metabolite PPD modulates the metabolism of amino acids and lipids, leading to the activation of the stress-sensing kinases GCN2 and PERK to induce Sesn2 expression, which promotes AMPK activation, autophagy, and metabolic health.
Panaxatriol derived from ginseng augments resistance exercised-induced protein synthesis via mTORC1 signaling in rat skeletal muscle.
Protective effect of ginsenoside metabolite compound K against diabetic nephropathy by inhibiting NLRP3 inflammasome activation and NF‐&kgr;B/p38 signaling pathway in high‐fat diet/streptozotocin‐induced diabetic mice
Antidiabetic Effects of Ginseng in Humans and Rodents
TLDR
Investigations in clonal beta-cells and non-beta-cells confirm that ginseng may protect against pancreatic beta-cell apoptosis and promote insulin secretion and glucose uptake, and based upon the sound evidence from cell lines and animal models, ginsENG appears to be a potent anti-diabetic supplement.
Identification and Characterization of a Ginsenoside-Transforming β-Glucosidase from Pseudonocardia sp. Gsoil 1536 and Its Application for Enhanced Production of Minor Ginsenoside Rg2(S)
TLDR
An enzymatic bioconversion method was developed to adopt the recombinant glycoside hydrolase (BglPC28), which is a ginsenoside-transforming recombinant β-glucosidase from Pseudonocardia sp.
...
1
2
3
...

References

SHOWING 1-10 OF 37 REFERENCES
Inhibition of lipid synthesis through activation of AMP kinase: an additional mechanism for the hypolipidemic effects of berberine Published, JLR Papers in Press, February 28, 2006.
TLDR
Findings indicate that BBR, in addition to upregulating the LDLR, inhibits lipid synthesis in human hepatocytes through the activation of AMPK, which could account for the strong reduction of plasma TGs observed with this drug in clinical trials.
Compound K, intestinal metabolite of ginsenoside, attenuates hepatic lipid accumulation via AMPK activation in human hepatoma cells.
TLDR
Taken together, AMPK mediates CK induced suppression and activation of SREBP1c and PPAR-alpha, respectively, and these effects seem to be one of antidiabetic and/or antihyperlipidemic mechanisms of CK in insulin-resistant HepG2 human hepatoma cells.
The ginsenoside Rg3 has a stimulatory effect on insulin signaling in L6 myotubes.
  • Min Kim, B. Ahn, K. Park
  • Biology, Medicine
    Biochemical and biophysical research communications
  • 2009
AMP-activated kinase reciprocally regulates triacylglycerol synthesis and fatty acid oxidation in liver and muscle: evidence that sn-glycerol-3-phosphate acyltransferase is a novel target.
TLDR
The data suggest that AICA riboside might inhibit sn-glycerol-3-phosphate acyltransferase (GPAT), which catalyses the committed step in the pathway of glycerolipid biosynthesis, and provide strong evidence that AMPK phosphorylates and inhibits mitochondrial GPAT.
Role of AMP-activated protein kinase in mechanism of metformin action.
TLDR
It is reported that metformin activates AMPK in hepatocytes; as a result, acetyl-CoA carboxylase (ACC) activity is reduced, fatty acid oxidation is induced, and expression of lipogenic enzymes is suppressed.
The Anti-diabetic Drugs Rosiglitazone and Metformin Stimulate AMP-activated Protein Kinase through Distinct Signaling Pathways*
TLDR
It is shown that incubation of muscle cells with the thiazolidinedione, rosiglitazone, leads to a dramatic increase in this ratio with the concomitant activation of AMPK, which raises the possibility that a number of the beneficial effects of the th Diazolidinediones could be mediated via activated AMPK.
Activation of AMP‐activated protein kinase in the liver: a new strategy for the management of metabolic hepatic disorders
TLDR
Findings reinforce the idea that pharmacological activation of AMPK may provide, through signalling and metabolic and gene expression effects, a new strategy for the management of metabolic hepatic disorders linked to type 2 diabetes and obesity.
The AMP-activated protein kinase activator AICAR does not induce GLUT4 translocation to transverse tubules but stimulates glucose uptake and p38 mitogen-activated protein kinases alpha and beta in skeletal muscle.
TLDR
The results suggest that AICAR increases muscle glucose uptake by two mechanisms: 1) inducing selective recruitment of GLUT4 to the plasma membrane, and 2) activating p38 MAPKalpha and beta, which may be involved in the activation ofGLUT4.
Induction of apoptosis by a novel intestinal metabolite of ginseng saponin via cytochrome c-mediated activation of caspase-3 protease.
Compound K enhances insulin secretion with beneficial metabolic effects in db/db mice.
TLDR
Compound K lowered the plasma glucose level by stimulating insulin secretion and this action was presumably associated with an ATP-sensitive K+ channel, and may suggest that CK could be developed as a therapeutic tool in type 2 diabetic patients with disability of insulin gland secretion and/or insulin resistance.
...
1
2
3
4
...