7-O-Methylaromadendrin Stimulates Glucose Uptake and Improves Insulin Resistance in Vitro

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  • Zhang Wei Yun
    Department of Pharmacology, College of Pharmacy, Chungnam National University
  • Lee Jung-Jin
    Department of Pharmacology, College of Pharmacy, Chungnam National University Institute of Drug Research & Development, Chungnam National University
  • Kim In-Su
    Department of Pharmacology, College of Pharmacy, Chungnam National University
  • Kim Yohan
    Department of Pharmacology, College of Pharmacy, Chungnam National University
  • Park Jeong-Sook
    Institute of Drug Research & Development, Chungnam National University Department of Physical Pharmacy, College of Pharmacy, Chungnam National University Graduate School of New Drug Discovery and Development, Chungnam National University
  • Myung Chang-Seon
    Department of Pharmacology, College of Pharmacy, Chungnam National University Institute of Drug Research & Development, Chungnam National University Graduate School of New Drug Discovery and Development, Chungnam National University

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The stimulation of glucose uptake into peripheral tissues is an important mechanism for the removal of glucose in blood and for the management of diabetes mellitus (DM). Since recent results have demonstrated the beneficial effects of flavonoids in relation to DM, this study was designed to examine the effects of 7-O-methylaromadendrin (7-O-MA), a flavonoid isolated from Inula viscosa, on glucose uptake into liver and fat tissue, and investigate the molecular mechanisms involved. 7-O-MA at 10 μM significantly stimulated insulin-induced glucose uptake measured by 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose (2-NBDG) in both human hepatocellular liver carcinoma (HepG2) cells and differentiated 3T3-L1 adipocytes. Adipocyte-specific fatty acid binding protein (aP2) gene expression was increased by 7-O-MA in adipocytes, and both gene and protein level of peroxisome proliferator-activated receptor γ2 (PPARγ2) was also increased. Moreover, 7-O-MA stimulated the reactivation of insulin-mediated phosphorylation of phosphatidylinositol 3-kinase (PI3K)-linked protein kinase B (Akt/PKB) and adenosine 5′-monophosphate-activated protein kinase (AMPK) in high glucose-induced, insulin-resistant HepG2 cells, and this effect was blocked by either LY294002, a PI3K inhibitor, or compound C, an AMPK inhibitor. Therefore, these results suggest that 7-O-MA might stimulate glucose uptake via PPARγ2 activation and improve insulin resistance via PI3K and AMPK-dependent pathways, and be a potential candidate for the management of type 2 DM.

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