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Relationship between Angiotensin-Converting Enzyme Gene Polymorphism and Insulin Resistance in Never-Treated Hypertensive Patients

Cardiovascular Diseases Unit, Clinical Pathology Laboratory (E.G.), Molecular Pathology Laboratory (N.P.), and Department of Medicina Sperimentale e Clinica G. Salvatore, University of Catanzaro, Magna Graecia, 88100 Catanzaro, Italy

Address all correspondence and requests for reprints to: Francesco Perticone, M.D., Dipartimento di Medicina Sperimentale e Clinica G. Salvatore, Policlinico Mater Domini, Via Tommaso Campanella, 88100 Catanzaro, Italy. E-mail: perticone{at}unicz.it

The association between angiotensin-converting enzyme (ACE) gene polymorphism and insulin resistance (IR) in hypertensive subjects remains controversial. Thus, we evaluated the possible association between IR and ACE gene polymorphism in a group of hypertensive, never-treated patients compared with that in a normotensive control group. We enrolled 200 (114 men and 86 women; age, 45.5 ± 4.7 yr) hypertensive patients and 96 (54 men and 42 women; age, 44.0 ± 4.7 yr) normotensive subjects. A double PCR assay was used to identify ACE genotypes. We determined fasting glucose and insulin by the glucose oxidase method and using a standard RIA technique. IR was estimated using the homeostasis model assessment (HOMA_IR). Both fasting glucose (5.0 ± 0.3 vs. 4.7 ± 0.3 mmol/L; P < 0.0001), insulin levels (12.3 ± 4.7 vs. 4.9 ± 1.5 µU/mL; P < 0.0001), and HOMA_IR (2.7 ± 1.1 vs. 1.1 ± 0.3; P < 0.0001) were significantly higher in hypertensive patients than in the normotensive control group. When we subdivided hypertensive patients according to ACE genotype, we observed that fasting insulin and HOMA_IR were 16.3 ± 3.3 and 3.6 ± 0.8 in the DD genotype, 9.4 ± 3.1 and 2.1 ± 0.7 in the ID genotype, and 8.3 ± 2.8 and 1.9 ± 0.7 µU/mL in the II group (P < 0.0001, by ANOVA). No significant differences were observed in the normotensive control group. In conclusion, we extended previous data regarding the relationship of hypertension and IR by demonstrating a dependence of this relationship upon the ACE gene polymorphism.

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