PMID: 18347976.-- Final full-text version of the paper available at: 10.1007/s10719-008-9118-8 or http://www.springerlink.com/content/41v66012055486r0/
The aim of this study is to test several biomarkers of inflammation, of endothelial dysfunction, glycated haemoglobin, and their reflection in arterial dilatation, in patients with type 2 diabetes mellitus and in their relatives, in order to demonstrate if relatives present markers as a form of precocious indicators of diabetes mellitus. Individuals between 30 and 55 years of age and without clinical arterial disease were divided in three groups: type 2 diabetes mellitus patients without complications (12 men and 18 women); first degree relatives of type 2 diabetes mellitus (14 men and 20 women); and control individuals (9 men and 16 women). Body composition was measured with a bioelectrical impedance analyzer and endothelial function with an eco-Doppler device. We determined glucose, insulin, C-peptide, glycated haemoglobin, fibrinogen, E-selectin, P-selectin, soluble intercellular cell adhesion molecule-1 (ICAM-1), soluble vascular cell adhesion molecule-1 (VCAM-1), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), C-reactive protein (CRP) in plasma. We also studied endothelium independent dilatation and endothelium dependent dilatation. The results: ICAM-1 and VCAM-1 were significantly higher in the diabetic group (237.5 ± 43.4 and 692.5 ± 168.6 ng/l) than in controls (197.4 ± 51.2 and 573.5 ± 121.1 ng/l, p = 0.011 and 0.013, respectively), but were not higher in the family group (224.5 ± 45.2 and 599.8 ± 150.4 ng/l). CRP was higher in the diabetic group (3.35 ± 3.27 mg/l) than in the other groups (1.28 ± 1.29 and 1.61 ± 1.54 mg/l, p = 0.002) and correlated with glycated haemoglobin. The non-endothelium mediated dilatation was lesser in the diabetic group than in the family group (17.3 ± 6.1 vs. 24 ± 8, p = 0.029) and controls. In conclusion patients with uncomplicated type 2 diabetes, but not their relatives, have biochemical markers of sub-clinical inflammation in relationship with glycated haemoglobin and dysfunction of the endothelial cells markers. In these patients endothelium independent dilatation is more affected than endothelium dependent dilatation.
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