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Impaired fasting blood glucose and circulating endothelial progenitor cell function (1072.4)
Author(s) -
Bammert Tyler,
Beckstrom Collin,
Diehl Kyle,
Kavlich Philip,
Greiner Jared,
Stauffer Brain,
DeSouza Christopher
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1072.4
Subject(s) - progenitor cell , medicine , impaired fasting glucose , endocrinology , basal (medicine) , endothelial progenitor cell , peripheral blood mononuclear cell , diabetes mellitus , type 2 diabetes , impaired glucose tolerance , biology , stem cell , in vitro , biochemistry , genetics
Impaired fasting blood glucose (IFG: 100‐125 mg/dL) is a risk factor for type 2 diabetes and confers cardiovascular risk. Functional impairment of circulating endothelial progenitor cells (EPCs) is linked to atherogenesis. We tested the hypothesis that IFG is associated with EPC dysfunction. Peripheral blood samples were collected from 22 adults (19 M/3 F): 10 normal fasting glucose (NFG; age: 57±3 yr; BMI: 29.7±1.4 kg/m2; glucose: 90±1 mg/dL) and 12 IFG (59±1 yr; 28.6±1.1 kg/m2; 104±1 mg/dL). Cells with phenotypic putative EPC characteristics were isolated from peripheral blood mononuclear cells and EPC clonogenic (colony forming unit [CFU] assay) and migratory (Boyden chamber) capacity as well as apoptotic susceptibility (intracellular active caspase‐3 concentrations) and angiogenic growth factor release (ELISA) were determined. EPC colony forming capacity was ~60% lower (p<0.05) in the IFG (10±3) vs NFG (23±6) group. Basal (0.31±0.1 vs 0.21±0.1 ng/mL) and staurosporine‐stimulated (2.9±0.3 vs 2.1±0.3 ng/mL) active caspase‐3 levels were markedly (~45%; p<0.05) higher in EPCs from IFG compared with NFG adults. There were no significant differences in EPC migration or release of angiogenic factors. These results suggest that impaired fasting glucose adversely affects the ability of EPCs to form colonies and resist apoptosis, potentially contributing to the increased cardiovascular risk with hyperglycemia.