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Ganoderma lucidum extract stimulates glucose uptake in L6 rat skeletal muscle cells

100%

Jung K. H. , Ha E. , Kim M.-J. , Uhm Y. K. , Kim H. K. , Hong S.-J. , Chung J.-H. , Yim S.-V.

Acta Biochimica Polonica

2006

tom 53

nr 3

597-601

The effect of Ganoderma lucidum extract on glucose uptake was studied in L6 rat skeletal muscle cells. G. lucidum extract increased glucose uptake about 2-fold compared to control. The extract stimulated the activity of phosphatidylinositol (PI) 3-kinase which is a major regulatory molecule in the glucose uptake pathway. About 7-fold increased activity of a PI 3-kinase was observed after treatment with G. lucidum extract, whereas PI 3-kinase inhibitor, LY294002, blocked the G. lucidum extract-stimulated PI 3-kinase activity in L6 skeletal muscle cells. Protein kinase B, a downstream mediator of PI 3-kinase, was also activated by G. lucidum extract. We then assessed the activity of AMP-activated protein kinase (AMPK), another regulatory molecule in the glucose uptake pathway. G. lucidum extract increased the phosphorylation level of both AMPK α1 and α2. Activity of p38 MAPK, a downstream mediator of AMPK, was also increased by G. lucidum extract. Taken together, these results suggest that G. lucidum extract may stimulate glucose uptake, through both PI 3-kinase and AMPK in L6 skeletal muscle cells thereby contributing to glucose homeostasis.

Recent advances in the role of AMP-activated protein kinase in metabolic reprogramming of metastatic cancer cells: targeting cellular bioenergetics and biosynthetic pathways for anti-tumor treatment

72%

Tyszka-Czochara M. , Konieczny P. , Majka M.

Journal of Physiology and Pharmacology

2018

tom 69

nr 3

Crosstalk between autophagy and proteasome protein degradation systems: possible implications for cancer therapy

72%

Wojcik S.

Folia Histochemica et Cytobiologica

2013

tom 51

nr 4

Effects of hyperthyroidism on lipid content and composition in oxidative and glycolytic muscles in rats

58%

Miklosz A. , Chabowski A. , Zendzian-Piotrowska M. , Gorski J.

Journal of Physiology and Pharmacology

2012

tom 63

nr 4

Activation of the metabolic sensor - AMP activated protein kinase reverses impairment of angiogenesis in aging myocardial microvascular endothelial cells. Implications for the aging heart

58%

Ahluwalia A. , Tarnawski A. S.

Journal of Physiology and Pharmacology

2011

tom 62

nr 5

Metformin-induced regulation of the intestinal D-glucose transporters

58%

Sakar Y. , Meddah B. , Faouzi M. A. , Cherrah Y. , Bado A. , Ducroc R.

Journal of Physiology and Pharmacology

2010

tom 61

nr 3

301-307

Metformin is an orally administered drug that lowers blood glucose and improves insulin sensitivity in patients with non insulin-dependent diabetes. Although the antihyperglycemic effect of metformin has been extensively studied, its cellular mechanism(s) of action (including the effect on enterocyte) remains to be defined. This study was designed to examine the effect of metformin on glucose transporters in enterocyte. Na+-dependent glucose transporter-1 (SGLT-1) activity was followed as glucose-induced short-circuit current (Isc) in Ussing chambers. The effect of metformin (10 µmol/L, 3 min) on transmural glucose transport was studied in isolated rat jejunal loops. Its impact on abundance of transporters SGLT-1 and GLUT2 in jejunal brush border membranes (BBM) and its effect on the phosphorylation of AMP-activated protein kinase (AMPK) 2 subunit was studied by western blot. Acute effect of metformin was also measured in vivo by oral glucose tolerance test (OGTT). Metformin markedly inhibited glucose-induced Isc (~77%) after mucosal addition. In addition, metformin reduced the glucose-induced abundance of SGLT-1 in BBM and increased those of GLUT2, concomitantly increasing the phosphorylation of intracellular AMPK2. This effect of metformin was also observed using non-metabolizable sugar 3-O-methyl glucose. Transmural glucose transport measured in vitro was increased by 22% under metformin. Finally, oral metformin markedly increased glucose tolerance in OGTT. In conclusion, metformin slightly increases intestinal glucose absorption by inducing a re-distribution of glucose transporters in BBM through AMPK control in enterocyte. In addition to its action to other splanchnic tissues, this could constitute a peripheral signal contributing to the beneficial effect of metformin on glucose tolerance.