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Purpose: Since diabetes and hypertension frequently occur together, it is thought that these conditions may have a common pathogenesis. This study was designed to evaluate the anti-diabetic function of the anti-hypertensive drug fimasartan on C2C12 mouseskeletal muscle and HepG2 human liver cells in a high glucose state. Materials and Methods: The anti-diabetic effects and mechanism of fimasartan were identified using Western blot, glucose uptaketests, oxygen consumption rate (OCR) analysis, adenosine 5'-triphosphate (ATP) enzyme-linked immunosorbent assay (ELISA),and immunofluorescence staining for diabetic biomarkers in C2C12 cells. Protein biomarkers for glycogenolysis and glycogenesiswere evaluated by Western blotting and ELISA in HepG2 cells. Results: The protein levels of phosphorylated 5' adenosine monophosphate-activated protein kinase (p-AMPK), p-AKT, insulinreceptor substrate-1 (IRS-1), and glucose transporter type 4 (Glut4) were elevated in C2C12 cells treated with fimasartan. These increaseswere reversed by peroxisome proliferator-activated receptor delta (PPARδ) antagonist. ATP, OCR, and glucose uptake wereincreased in cells treated with 200 μM fimasartan. Protein levels of glycogen phosphorylase, glucose synthase, phosphorylated glycogensynthase, and glycogen synthase kinase-3 (GSK-3) were decreased in HepG2 cells treated with fimasartan. However, theseeffects were reversed following the addition of the PPARδ antagonist GSK0660. Conclusion: In conclusion, fimasartan ameliorates deteriorations in glucose metabolism as a result of a high glucose state by regulatingPPARδ in skeletal muscle and liver cells.
