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

Authors
  • Kim, Kyung-Soo1
  • Choi, Yeon Kyung2
  • Kim, Mi Jin2
  • Hwang, Jung Wook2
  • Min, Kyunghoon3
  • Jung, Sang Youn1
  • Kim, Soo-Kyung1
  • Choi, Yong-Soo2
  • Cho, Yong-Wook1
  • 1 Department of Internal Medicine, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Korea. , (North Korea)
  • 2 Department of Biotechnology, CHA University, Seongnam, Korea. , (North Korea)
  • 3 Department of Rehabilitation Medicine, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam, Korea. , (North Korea)
Type
Published Article
Journal
Diabetes & metabolism journal
Publication Date
Mar 01, 2021
Volume
45
Issue
2
Pages
260–269
Identifiers
DOI: 10.4093/dmj.2019.0191
PMID: 32662257
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

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

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