Bone Marrow-Derived Mesenchymal Stem Cells Restored High-Fat-Fed Induced Hyperinsulinemia in Rats at Early Stage of Type 2 Diabetes Mellitus

• Published in: Cell transplantation Vol. 29; p. 963689720904628
• Main Authors: Li, Gongchi, Peng, Han, Qian, Shen, Zou, Xinhua, Du, Ye, Wang, Zhi, Zou, Lijun, Feng, Zibo, Zhang, Jing, Zhu, Youpeng, Liang, Huamin, Li, Binghui
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01.01.2020; Sage Publications Ltd; SAGE Publishing
• Subjects: AKT protein; Animals; Blotting, Western; Bone marrow; Bone Marrow Cells - cytology; Cells, Cultured; Diabetes; Diabetes mellitus (non-insulin dependent); Diet, High-Fat - adverse effects; Glucose - metabolism; Hyperglycemia - etiology; Hyperglycemia - therapy; Hyperinsulinemia; Hyperinsulinism - etiology; Hyperinsulinism - therapy; Immunohistochemistry; Inflammation; Insulin; Insulin - metabolism; Insulin receptor substrate 1; Insulin resistance; Interleukin 6; Islet cells; Kinases; Liver diseases; Male; Mesenchymal Stem Cell Transplantation - methods; Mesenchymal stem cells; Mesenchymal Stem Cells - cytology; Mesenchymal Stem Cells - physiology; Original; Pancreas; Protein kinase; Rats; Rats, Sprague-Dawley; Stem cell transplantation; Stem cells; Tumor necrosis factor-α; type 2 diabetes mellitus; lipometabolic disorder; insulin resistance; mesenchymal stem cells; high fat diet
• ISSN: 0963-6897; 1555-3892
• DOI: 10.1177/0963689720904628

Numerous studies have proposed the transplantation of mesenchymal stem cells (MSCs) in the treatment of typical type 2 diabetes mellitus (T2DM). We aimed to find a new strategy with MSC therapy at an early stage of T2DM to efficiently prevent the progressive deterioration of organic dysfunction. Using the high-fat-fed hyperinsulinemia rat model, we found that before the onset of typical T2DM, bone marrow-derived MSCs (BM-MSCs) significantly attenuated rising insulin with decline in glucose as well as restored lipometabolic disorder and liver dysfunction. BM-MSCs also favored the histological structure recovery and proliferative capacity of pancreatic islet cells. More importantly, BM-MSC administration successfully reversed the abnormal expression of insulin resistance-related proteins including GLUT4, phosphorylated insulin receptor substrate 1, and protein kinase Akt and proinflammatory cytokines IL-6 and TNFα in liver. These findings suggested that MSCs transplantation during hyperinsulinemia could prevent most potential risks of T2DM for patients.