Decaffeinated green tea extract regulates glucose metabolism in insulinsensitive cell lines
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Impairment of glucose and lipid metabolism are markers of insulin resistance, obesity, and type 2 diabetes (T2D). Green tea showed numerous potential biological activities and health benefits including amelioration this impairment, however, the underpinning mechanism is not yet fully understood. Therefore, the effect of green tea extract on glucose uptake and utilisation in 3T3-L1 (adipocyte), AML12 (hepatocyte), and C2C12 (myocyte), and the possible mechanism of this effect were investigated. 2-NBDG uptake in the presence of adenosine 5’monophosphate-activated protein kinase (AMPK) and protein kinase B (Akt) inhibitors, hepatic glycogen, adipocytes triglyceride, and glycerol released, cell viability, and metabolic gene expression were assessed. Green tea upregulated expression of glucose transporter 4 and 2 (GLUT4, 2) and therefore increased glucose uptake in all cell lines. This effect was suppressed in adipocytes and hepatocytes by Akt inhibitor, while AMPK inhibitor suppressed glucose uptake in myocytes. Furthermore, Green tea activated glycogen synthase (GyS1) gene and increased hepatic glycogen formation accordingly, alongside reduced gluconeogenesis activity gene glucose 6 phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK). A remarkable reduction in cellular triglyceride and glycerol released from 3T3-L1 were observed, suggesting suppressed adipogenesis and lipolysis. This inhibitory effect attributed to downregulation of CCAAT-enhancer-binding protein alpha (C/EBPα), sterol regulatory element binding protein 1c (SREPB1c), fatty acid synthase (FASN), fatty acid binding protein 4 (FABP4), and lipoprotein lipase (LPL) gene expressions. Finally, green tea could regulate glucose and lipid metabolism through activating phosphoinositide 3-kinase (PI3K)/Akt and AMPK and their downstream signalling, and therefore could be a potential anti-obesity and anti-diabetic agent.
Green tea, glucose metabolism, lipid metabolism, 3T3-L1, AML12, C2C12.