Fimasartan Ameliorates Deteriorations in Glucose Metabolism in a High Glucose State by Regulating Skeletal Muscle and Liver Cellsopen access
- Authors
- Jang, Yoo Na; Lee, Yong Jik; Han, Yoon Mi; Kim, Hyun Min; Seo, Hong Seog; Jeong, Ji Hoon; Park, Seung Yeon; Jung, Tae Woo
- Issue Date
- Jun-2022
- Publisher
- YONSEI UNIV COLL MEDICINE
- Keywords
- Fimasartan; angiotensin II type 1 receptor blocker; glucose metabolism; PPAR delta
- Citation
- YONSEI MEDICAL JOURNAL, v.63, no.6, pp.530 - 538
- Journal Title
- YONSEI MEDICAL JOURNAL
- Volume
- 63
- Number
- 6
- Start Page
- 530
- End Page
- 538
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/85001
- DOI
- 10.3349/ymj.2022.63.6.530
- ISSN
- 0513-5796
- Abstract
- Purpose: Since diabetes and hypertension frequently occur together, it is thought that these conditions may have a common patho-genesis. 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 (PPAR delta) antagonist. ATP, OCR, and glucose uptake were increased in cells treated with 200 mu M 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 PPAR delta antagonist GSK0660. Conclusion: In condusion, fimasartan ameliorates deteriorations in glucose metabolism as a result of a high glucose state by regulating PPAR delta in skeletal muscle and liver cells.
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