Introduction: People with type 1 diabetes (T1D) have an increased risk of developing cardiovascular disease. Endothelial cell dysfunction is thought to be a factor in this increased risk but underlying cellular mechanisms related to vasodilation, inflammation and oxidative stress are unknown.
Methods: Participants with T1D (n= 25) and non-T1D (n=20) were categorized into groups of high (≥80) or low (<15 AU) coronary artery calcium (CAC) , measured by computed tomography. Protein expression was assessed for endothelial Nitric Oxide Synthase [eNOS], estrogen receptors (ER) α and ER-β (women only) , nuclear factor [NF]κβ and nicotinamide adenine dinucleotide phosphate [NADPH] using quantitative immunofluorescence in peripheral venous endothelial cells harvested by endovascular biopsy. SphygmoCor Pulse Wave Velocity (PWV) measured arterial stiffness. Linear regression was used to test associations of high vs. low CAC and T1D with proteins of interest. All models included age, sex, CAC and diabetes.
Results: As shown in table 1, eNOS and NADPH were lower and NFκβ and Nitrotyrosine [NT] were higher in T1D compared to non-T1D participants with low CAC. Among T1D, PWV was higher in those with high vs. low CAC. Among non-T1D participants, eNOS was lower and NT and ER-α were lower in those with high vs. low CAC.
Conclusions: T1D is associated with adverse endothelial proteins that may contribute to endothelial dysfunction and vascular disease.
H.K.Wise: None. A.Keshawarz: None. K.Moreau: None. J.K.Snell-bergeon: Stock/Shareholder; GlaxoSmithKline plc.