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ORIGINAL ARTICLE
Year : 2015  |  Volume : 11  |  Issue : 41  |  Page : 74-81

The molecular basis of the antidiabetic action of quercetin in cultured skeletal muscle cells and hepatocytes


1 Department of Pharmacology, Natural Health Products and Metabolic Diseases Laboratory, Université de Montréal, Montreal, QC; Canadian Institutes of Health Research Team in Aboriginal Antidiabetic Medicines and Montreal Diabetes Research Center, Canada; Department of Pharmacognosy, University of Beni seuf, Beni seuf, Egypt
2 Department of Pharmacology, Natural Health Products and Metabolic Diseases Laboratory, Université de Montréal, Montreal, QC; Canadian Institutes of Health Research Team in Aboriginal Antidiabetic Medicines and Montreal Diabetes Research Center, Canada
3 Department of Biology, York University, Toronto, Ontario, Canada

Correspondence Address:
Pierre S Haddad
Department of Pharmacology, Université de Montréal, P.O. Box 6128, Station Centre Ville, Montréal, Québec, H3C 3J7 Canada

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0973-1296.149708

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Background: Quercetin is universally distributed in the plant kingdom and is the most abundant flavonoid in the human diet. In a previous study, we have reported that quercetin stimulated glucose uptake in cultured C2C12 skeletal muscle through an insulin-independent mechanism involving adenosine monophosphate-activated protein kinase (AMPK). AMPK is a key regulator of the whole body-energy homeostasis. In skeletal muscle, activation of AMPK increases glucose uptake through the stimulation of the glucose transporter GLUT4 translocation to the plasma membrane. In liver, AMPK decreases glucose production mainly through the downregulation of the key gluconeogenesis enzymes such as phosphoenolpyruvate carboxylase (PEPCK) and Glucose -6-phosphate (G6Pase). Objective: To study the effect of quercetin on glucose homeostasis in muscle and liver. Materials and Methods: L6 skeletal muscle cells, murine H4IIE and human HepG2 hepatocytes were treated with quercetin (50 μM) for 18 h. Results: An 18 h treatment with quercetin (50 μM) stimulated AMPK and increased GLUT4 translocation and protein content in cultured rat L6 skeletal muscle cells. On the other hand, we report that quercetin induced hepatic AMPK activation and inhibited G6pase in H4IIE hepatocytes. Finally, we have observed that quercetin exhibited a mild tendency to increase the activity of glycogen synthase (GS), the rate-limiting enzyme of glycogen synthesis, in HepG2 hepatocytes. Conclusions: Overall, these data demonstrate that quercetin positively influences glucose metabolism in the liver and skeletal muscle, and therefore appear to be a promising therapeutic candidate for the treatment of in type 2 diabetes.


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