4.5 Article

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

期刊

DIABETES & METABOLISM JOURNAL
卷 45, 期 2, 页码 260-+

出版社

KOREAN DIABETES ASSOC
DOI: 10.4093/dmj.2019.0191

关键词

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

资金

  1. Korean Diabetes Association [2016F-2]
  2. [NRF-2018R1C1B5042633]

向作者/读者索取更多资源

UC-MSC-CM improves insulin resistance in C2C12 cells through multiple mechanisms, including increasing glucose uptake, membrane GLUT4 expression, restoring insulin signaling pathway, and enhancing mitochondrial contents and functions.
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. Mitochondria' contents evaluated by mitochondrial transcription factor A, mitochondria' 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 mitochondria' reactive oxygen species and increased fatty acid oxidation and mitochondria' 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.

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