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Umbilical Cord-Mesenchymal Stem Cell-Conditioned Medium Improves Insulin Resistance in C2C12 Cell

Diabetes & Metabolism Journal 2021년 45권 2호 p.260 ~ 269
김경수, 최연경, 김미진, 황정욱, 민경훈, 정상윤, 김수경, 최용수, 조용욱,
소속 상세정보
김경수 ( Kim Kyung-Soo ) - CHA University School of Medicine CHA Bundang Medical Center Department of Internal Medicine
최연경 ( Choi Yeon-Kyung ) - CHA University Department of Biotechnology
김미진 ( Kim Mi-Jin ) - CHA University Department of Biotechnology
황정욱 ( Hwang Jung-Wook ) - CHA University Department of Biotechnology
민경훈 ( Min Kyung-Hoon ) - CHA University School of Medicine CHA Bundang Medical Center Department of Rehabilitation Medicine
정상윤 ( Jung Sang-Youn ) - CHA University School of Medicine CHA Bundang Medical Center Department of Internal Medicine
김수경 ( Kim Soo-Kyung ) - CHA University School of Medicine CHA Bundang Medical Center Department of Internal Medicine
최용수 ( Choi Yong-Soo ) - CHA University Department of Biotechnology
조용욱 ( Cho Yong-Wook ) - CHA University School of Medicine CHA Bundang Medical Center Department of Internal Medicine

Abstract


Background: Umbilical cord-mesenchymal stem cell-conditioned medium (UC-MSC-CM) has emerged as a promising cell-free therapy. The aim of this study was to explore the therapeutic effects of UC-MSC-CM on insulin resistance in C2C12 cell.

Methods: Insulin resistance was induced by palmitate. Effects of UC-MSC-CM on insulin resistance were evaluated using glucose uptake, glucose transporter type 4 (GLUT4) translocation, the insulin-signaling pathway, and mitochondrial contents and functions in C2C12 cell.

Results: Glucose uptake was improved by UC-MSC-CM. UC-MSC-CM treatment increased only in membranous GLUT4 expression, not in cytosolic GLUT4 expression. It restored the insulin-signaling pathway in insulin receptor substrate 1 and protein kinase B. Mitochondrial contents evaluated by mitochondrial transcription factor A, mitochondrial DNA copy number, and peroxisome proliferator-activated receptor gamma coactivator 1-alpha were increased by UC-MSC-CM. In addition, UC-MSC-CM significantly decreased mitochondrial reactive oxygen species and increased fatty acid oxidation and mitochondrial membrane potential. There was no improvement in adenosine triphosphate (ATP) contents, but ATP synthesis was improved by UC-MSC-CM. Cytokine and active factor analysis of UC-MSC-CM showed that it contained many regulators inhibiting insulin resistance.

Conclusion: UC-MSC-CM improves insulin resistance with multiple mechanisms in C2C12 cell.

키워드

Culture media, conditioned; Diabetes mellitus; Insulin resistance; Mesenchymal stem cells; Mitochondria; Muscles; Umbilical cord; Wharton jelly

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