Yonsei Med J.
2022 Jun;63(6):530-538. 10.3349/ymj.2022.63.6.530.
Fimasartan Ameliorates Deteriorations in Glucose Metabolism in a High Glucose State by Regulating Skeletal Muscle and Liver Cells
- Affiliations
-
- 1Cardiovascular Center, Korea University Guro Hospital, Seoul, Korea.
- 2Department of Medicine, Graduate School, College of Medicine, Chung-Ang University, Seoul, Korea.
- 3Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Korea.
- 4Laboratory of Genomics and Translational Medicine, Department of Internal Medicine, Gachon University College of Medicine, Incheon, Korea.
- 5Department of Medical Science, Korea University College of Medicine, Seoul, Korea.
- 6Department of Global Innovative Drugs, Graduate School of Chung-Ang University, Seoul, Korea.
- KMID: 2530373
- DOI: http://doi.org/10.3349/ymj.2022.63.6.530
Abstract
- 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 mouse skeletal 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 uptake tests, 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 glycogenesis were 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, insulin receptor substrate-1 (IRS-1), and glucose transporter type 4 (Glut4) were elevated in C2C12 cells treated with fimasartan. These increases were reversed by peroxisome proliferator-activated receptor delta (PPARδ) antagonist. ATP, OCR, and glucose uptake were increased in cells treated with 200 μM fimasartan. Protein levels of glycogen phosphorylase, glucose synthase, phosphorylated glycogen synthase, and glycogen synthase kinase-3 (GSK-3) were decreased in HepG2 cells treated with fimasartan. However, these effects 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 regulating PPARδ in skeletal muscle and liver cells.
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