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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:431-432
doi: 10.1161/01.ATV.0000196552.84475.fc
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:431.)
© 2006 American Heart Association, Inc.


Letters to the Editor

Letter to the Editor

Insulin Resistance and Increased Intimal Medial Thickness in Glucose Tolerant Offspring of Type 2 Diabetic Subjects Carrying the D298D Genotype of Endothelial Nitric Oxide Synthase

Stefano Rizza; Manfredi Tesauro; Marina Cardellini; Rossella Menghini; Alfonso Bellia; Maria Adelaide Marini; Davide Lauro; Paolo Sbraccia; Giorgio Sesti; Renato Lauro; Massimo Federici

From the Department of Internal Medicine, University of Rome Tor Vergata, Rome, Italy., Correspondence to Dr Massimo Frederici, Department of Internal Medicine, University of Rome Tor Vergata, Via Montpellier 1, 00133 Rome, Italy. E-mail federicm@uniroma2.it


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

Endothelial nitric oxide synthase (eNOS) deficiency was found to affect insulin sensitivity and vascular homeostasis in animal models.1,2 Blood flow regulation by endothelial NO was suggested to modulate glucose uptake in the skeletal muscle.3 Therefore, it is possible that also in human subjects defects in eNOS activation or levels could affect insulin sensitivity.3 The D298D eNOS variant reduces eNOS protein half-life under stress conditions4 and it has been associated to increased cardiovascular disease (CVD) risk.5 The aim of present study was to assess whether among healthy offspring of patients with type 2 diabetes mellitus (T2DM) carriers of the D298D genotype are characterized by insulin resistance and early signs of atherosclerosis.

We recruited 142 young white offspring of T2DM with these inclusion criteria: age <45 years, 1 parent affected by T2DM, normal glucose tolerance (fasting plasma glucose <110 mg/dL; 2-hour plasma glucose <140 mg/dL), body mass index (BMI) less than 30 kg/m2, and absence of diseases or drugs able to modify glucose metabolism.

The phenotypization protocol, performed in all patients, was previously described and included blood sampling, blood pressure evaluation, oral glucose tolerance test and euglycemic hyperinsulinemic clamp technique.6 Moreover, high resolution B-mode ultrasound (HDI 3000 ultrasound system) was utilized to measure intima-media thickness (IMT). Briefly, the anterior, lateral, and posterolateral projections were used to image longitudinally the right and left common carotid arteries. At each projection, 3 determinations of IMT were made at 2 cm proximal to the bulb, at the site of greatest thickness. The . . . [Full Text of this Article]




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