Metformin improves circulating endothelial cells and endothelial progenitor cells in type 1 diabetes: MERIT study

• Published in: Cardiovascular diabetology 2016-08, Vol.15 (1), p.116-116, Article 116
• Main Authors: Ahmed, Fahad W, Rider, Rachel, Glanville, Michael, Narayanan, Kilimangalam, Razvi, Salman, Weaver, Jolanta U
• Format: Article
• Language: English
• Subjects: Adult; Biomarkers - blood; Blood Glucose - drug effects; Blood Glucose - metabolism; Cell Adhesion - drug effects; Cell Count; Cells, Cultured; Colony-Forming Units Assay; Diabetes Mellitus, Type 1 - blood; Diabetes Mellitus, Type 1 - drug therapy; Diabetes Mellitus, Type 1 - pathology; Drug Therapy, Combination; Endothelial Cells - drug effects; Endothelial Cells - metabolism; Endothelial Cells - pathology; Endothelial Progenitor Cells - drug effects; Endothelial Progenitor Cells - metabolism; Endothelial Progenitor Cells - pathology; England; Female; Fibronectins - metabolism; Humans; Hypoglycemic Agents - adverse effects; Hypoglycemic Agents - therapeutic use; Insulin - therapeutic use; Male; Metformin - adverse effects; Metformin - therapeutic use; Middle Aged; Original Investigation; Phenotype; Time Factors; Treatment Outcome
• ISSN: 1475-2840; 1475-2840
• DOI: 10.1186/s12933-016-0413-6

Type 1 diabetes is associated with increased cardiovascular disease (CVD). Decreased endothelial progenitor cells (EPCs) number plays a pivotal role in reduced endothelial repair and development of CVD. We aimed to determine if cardioprotective effect of metformin is mediated by increasing circulating endothelial progenitor cells (cEPCs), pro-angiogenic cells (PACs) and decreasing circulating endothelial cells (cECs) count whilst maintaining unchanged glycemic control. This study was an open label and parallel standard treatment study. Twenty-three type 1 diabetes patients without overt CVD were treated with metformin for 8 weeks (treatment group-TG). They were matched with nine type 1 diabetes patients on standard treatment (SG) and 23 age- and sex-matched healthy volunteers (HC). Insulin dose was adjusted to keep unchanged glycaemic control. cEPCs and cECs counts were determined by flow cytometry using surface markers CD45(dim)CD34(+)VEGFR-2(+) and CD45(dim)CD133(-)CD34(+)CD144(+) respectively. Peripheral blood mononuclear cells were cultured to assess changes in PACs number, function and colony forming units (CFU-Hill's colonies). At baseline TG had lower cEPCs, PACs, CFU-Hills' colonies and PACs adhesion versus HC (p