Umbilical Cord-Mesenchymal Stem Cell-Conditioned Medium Improves Insulin Resistance in C2C12 Cell
| Autor: | Kyunghoon Min, Yong-Soo Choi, Soo Kyung Kim, Yeon Kyung Choi, Kyung Soo Kim, Jung Wook Hwang, Sang Youn Jung, Yong Wook Cho, Mi Jin Kim |
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| Rok vydání: | 2021 |
| Předmět: |
Endocrinology
Diabetes and Metabolism Glucose uptake wharton jelly 030209 endocrinology & metabolism 030204 cardiovascular system & hematology Mitochondrion lcsh:Diseases of the endocrine glands. Clinical endocrinology 03 medical and health sciences 0302 clinical medicine Insulin resistance insulin resistance medicine Humans Insulin culture media conditioned mesenchymal stem cells lcsh:RC648-665 biology business.industry Glucose transporter TFAM medicine.disease IRS1 Cell biology mitochondria Cytosol Basic Research diabetes mellitus umbilical cord biology.protein Original Article muscles business GLUT4 |
| Zdroj: | Diabetes & Metabolism Journal, Vol 45, Iss 2, Pp 260-269 (2021) Diabetes & Metabolism Journal |
| ISSN: | 2233-6087 2233-6079 |
| DOI: | 10.4093/dmj.2019.0191 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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