Epigallocatechin-3-O-gallate (EGCG) protects the insulin sensitivity in rat L6 muscle cells exposed to dexamethasone condition

Zhang, Z.F.; Li, Q.; Liang, Jing; Dai, Xiaoqian; Ding, Yi; Wang, J.B.; Li, Y.

doi:10.1016/j.phymed.2009.09.007

Cited by 92 publications

(68 citation statements)

References 21 publications

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“…C2C12 myotubes were pretreated with 100 nmol/L wortmannin or 2 lmol/L compound C for 6 h before being treated with 20 lmol/L myricetin for 12 h. The phosphorylation level of Akt and AMPK was determined via western blot analysis (c). Asterisk represented statistically significant difference from control group, p \ 0.05 were stimulated with the same dosage of insulin used in the recent study from our laboratory [23]. As expected, lowdose insulin (100 nmol/L, 1 h) stimulation increased glucose uptake remarkably (p \ 0.05).…”

Section: Myricetin Increased Glucose Uptake By the Activation Of Akt supporting

confidence: 68%

Myricetin attenuates hyperinsulinemia-induced insulin resistance in skeletal muscle cells

Ding

Dai

Zhang

et al. 2012

Eur Food Res Technol

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Previous studies have shown that hyperinsulinemia is not only a marker of insulin resistance, but also the causative factor of peripheral tissue insulin resistance. It also has been suggested that prolonged high-dose insulin treatment can mimic the effects of hyperinsulinemia and exacerbate insulin resistance in skeletal muscle cells. However, how to prevent or reverse insulin resistance induced by hyperinsulinemia remains largely unclear.In the past few decades, the use of myricetin as an antidiabetic agent has gained much attention, but little information is available regarding the effects of myricetin on glucose uptake and hyperinsulinemia-induced insulin resistance in skeletal muscle cells. The present study focuses on the effect of myricetin on insulin signaling in skeletal muscle cell line C2C12 myotubes. Initially, the effect of myricetin under normal condition was determined. We found that myricetin's enhancement in glucose uptake coincided with both protein kinase B (Akt) and AMPactivated protein kinase (AMPK) activities. After that, the role of hyperinsulinemia was investigated. It was showed that prolonged high-dose insulin treatment inhibited both Akt and AMPK activities. As the results, the low-dose insulin stimulation of glucose uptake was inhibited by hyperinsulinemia. However, the treatment of myricetin improved low-dose insulin-stimulated glucose uptake in the hyperinsulinemic state, and this effect essentially depended on the AMPK signal pathway. Together, our data suggest a putative link between hyperinsulinemia and insulin resistance in C2C12 myotubes, and the myricetin treatment stimulates glucose uptake and attenuates insulin resistance.

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Section: Myricetin Increased Glucose Uptake By the Activation Of Akt supporting

confidence: 68%

Myricetin attenuates hyperinsulinemia-induced insulin resistance in skeletal muscle cells

Ding

Dai

Zhang

et al. 2012

Eur Food Res Technol

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“…Several studies revealed that GCs inhibit insulin signaling in 3T3-L1 adipocytes, L6 myotubes, and HepG2 hepatocytes (30,32,33). In this study, dexamethasone inhibited the phosphorylation of Akt and the glucose uptake induced by insulin in 3T3-L1 adipocytes, HepG2 hepatocytes, and C2C12 myotubes in vitro.…”

Section: Discussionsupporting

confidence: 49%

Role of Plasminogen Activator Inhibitor-1 in Glucocorticoid-Induced Diabetes and Osteopenia in Mice

et al. 2014

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Long-term use of glucocorticoids (GCs) causes numerous adverse effects, including glucose/lipid abnormalities, osteoporosis, and muscle wasting. The pathogenic mechanism, however, is not completely understood. In this study, we used plasminogen activator inhibitor-1 (PAI-1)–deficient mice to explore the role of PAI-1 in GC-induced glucose/lipid abnormalities, osteoporosis, and muscle wasting. Corticosterone markedly increased the levels of circulating PAI-1 and the PAI-1 mRNA level in the white adipose tissue of wild-type mice. PAI-1 deficiency significantly reduced insulin resistance and glucose intolerance but not hyperlipidemia induced by GC. An in vitro experiment revealed that active PAI-1 treatment inhibits insulin-induced phosphorylation of Akt and glucose uptake in HepG2 hepatocytes. However, this was not observed in 3T3-L1 adipocytes and C2C12 myotubes, indicating that PAI-1 suppressed insulin signaling in hepatocytes. PAI-1 deficiency attenuated the GC-induced bone loss presumably via inhibition of apoptosis of osteoblasts. Moreover, the PAI-1 deficiency also protected from GC-induced muscle loss. In conclusion, the current study indicated that PAI-1 is involved in GC-induced glucose metabolism abnormality, osteopenia, and muscle wasting in mice. PAI-1 may be a novel therapeutic target to mitigate the adverse effects of GC.

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“…In all cases mean ± SD were compared using independent samples t test for P \ 0.05 (CI = 0.95) out the effects of cholorogenic acid, frolic acid and berbein in L6 myotubes; the effect of mentioned components was compared with the effect of metformin and thiazolidindiones; cholorogenic and frolic acid did enhance GLUT4 transcription without and with a PI3-K pathway independent and dependent mechanisms respectively [32]. Another research team has reported Epigallocatechin-3-O-gallate (EGCG), a phenolic component of green tea, increases GLUT4 translocation from cytosolic compartments to the CM in L6 myotubes; this effect was an adenosine monophosphate protein kinase (AMPK) and PI3-K dependent event [33]. Also we have shown that HACE increases GLUT4 contents of CM in C2C12 myotubes.…”

Section: Resultsmentioning

confidence: 99%

Hydro-Alcoholic Cinnamon Extract, Enhances Glucose Transporter Isotype-4 Translocation from Intracellular Compartments into the Cytoplasmic Membrane of C2C12 Myotubes

et al. 2012

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Cinnamon has been used as an anti-diabetic agent for centuries but only in recent few years its mechanism of action has been under investigation. Previous studies showed that cinnamon might exert its anti-diabetic effect via increasing glucose transporter isotype-4 (GLUT4) gene and glycoprotein contents in fat cells. To study if hydro-alcoholic cinnamon extract (HACE) enhances GLUT4 translocation from intracellular compartments of nuclear or endoplasmic reticulum membranes (N/ER) into the cytoplasmic membrane (CM). C2C12 myoblastic cell line were seeded in DMEM plus 20 % FBS and differentiated to myotubes using 2 % horse serum. After myotubes formation, 100 or 1,000 lg/ml HACE, as intervention, and as control 1 % DMSO were added for 3 h. Cells were washed and homogenized followed by ultracentrifuge fractionation, protein separation by SDS-PAGE and GLUT4 detection using semi-quantitative Western blotting. Data analysis was done by two-independent samples t test for comparison of mean ± SD of GLUT4 percent in categories. GLUT4 contents were higher in CM of groups 100 and 1,000 lg/ml HACE and lower in 1 % DMSO treated myotubes (CI = 0.95, P \ 0.05). For N/ER reverse results were obtained (CI = 0.95, P \ 0.05). As our results have shown HACE induces GLUT4 translocation from intra-cell into cell surface. We conclude that cinnamon maybe a choice of type-2 diabetes mellitus treatment because its extract enhances GLUT4 contents in CM where it facilitates glucose entrance into the cell. However it is necessary to trace the signaling pathways which are activated by HACE in muscular tissue.

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Epigallocatechin-3-O-gallate (EGCG) protects the insulin sensitivity in rat L6 muscle cells exposed to dexamethasone condition

Cited by 92 publications

References 21 publications

Myricetin attenuates hyperinsulinemia-induced insulin resistance in skeletal muscle cells

Myricetin attenuates hyperinsulinemia-induced insulin resistance in skeletal muscle cells

Role of Plasminogen Activator Inhibitor-1 in Glucocorticoid-Induced Diabetes and Osteopenia in Mice

Hydro-Alcoholic Cinnamon Extract, Enhances Glucose Transporter Isotype-4 Translocation from Intracellular Compartments into the Cytoplasmic Membrane of C2C12 Myotubes

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