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Diabetes 50:159-165, 2001
© 2001 by the American Diabetes Association, Inc.

Obesity and Body Fat Distribution Induce Endothelial Dysfunction by Oxidative Stress

Protective Effect of Vitamin C

Francesco Perticone, Roberto Ceravolo, Mafalda Candigliota, Giorgio Ventura, Saverio Iacopino, Flora Sinopoli, and Pier L. Mattioli

From the Cardiovascular Disease Unit, Department of Experimental and Clinical Medicine G. Salvatore, University of Catanzaro Magna Graecia, Catanzaro, Italy.

Address correspondence and reprint requests to Francesco Perticone, MD, Dipartimento di Medicina Sperimentale e Clinica G. Salvatore, Policlinico Mater Domini—Via T. Campanella, 88100 Catanzaro, Italy. E-mail: perticone{at}unicz.it .

Endothelial dysfunction has been reported in obese subjects, but its mechanism has not been elucidated. We have therefore investigated 1) the possible relationship among BMI, waist-to-hip ratio (WHR), and endothelium-dependent vasodilation and 2) whether oxidative stress participates in endothelial dysfunction. We recruited 76 healthy subjects (50 men and 26 women aged 21-45 years) and measured their BMI (kg/m2), WHR, and insulin resistance (IR) estimated by the homeostasis model assessment (HOMA). Endothelium-dependent and -independent vasodilation were assessed by increasing doses of acetylcholine (ACh) (7.5, 15, and 30 µg · ml-1 · min-1) and sodium nitroprusside (SNP) (0.8, 1.6, and 3.2 µg · ml-1 · min-1) during saline and vitamin C coinfusion (24 mg/min). The effects of cyclooxygenase activity were evaluated by a dose-response curve to intrabrachial coinfusion of ACh and indomethacin (500 µg/min). Three different groups have been identified according to their BMI: group A (BMI <25), consisting of 10 men and 5 women; group B (BMI between 25 and 29), consisting of 16 men and 8 women; and group C (BMI >=30), consisting of 24 men and 13 women. Obese subjects had significantly lower forearm blood flow (FBF) during ACh infusions (means ± SD): 19.8 ± 2.8, 10.8 ± 2.7, and 6.5 ± 1.8 ml · 100 ml-1 tissue · min-1 (P < 0.0001) for groups A, B, and C, respectively. SNP caused comparable increments in FBF in all groups. Regression analysis revealed a significant negative correlation between BMI (r = -0.676, P < 0.0001), WHR (r = -0.631, P < 0.0001), fasting insulin (r = -0.695, P < 0.0001), HOMA-IR (r = -0.633, P < 0.0001), and percent peak increase in FBF during ACh infusion. In obese subjects, both vitamin C and indomethacin increased the impaired vasodilating response to ACh, whereas the SNP effect was unchanged. In conclusion, in obese subjects, ACh-stimulated vasodilation is blunted, and the increase in FBF is inversely related to BMI, WHR, fasting insulin, and HOMA-IR. The effects of both vitamin C and indomethacin on impaired ACh-stimulated vasodilation support the hypothesis that oxidative stress contributes to endothelial dysfunction in human obesity.


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