Relationship between angiotensin-converting enzyme gene polymorphism and insulin resistance in never-treated hypertensive patients

Citation
F. Perticone et al., Relationship between angiotensin-converting enzyme gene polymorphism and insulin resistance in never-treated hypertensive patients, J CLIN END, 86(1), 2001, pp. 172-178
Citations number
53
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
86
Issue
1
Year of publication
2001
Pages
172 - 178
Database
ISI
SICI code
0021-972X(200101)86:1<172:RBAEGP>2.0.ZU;2-H
Abstract
The association between angiotensin-converting enzyme (ACE) gene polymorphi sm and insulin resistance (IR) in hypertensive subjects remains controversi al. Thus, we evaluated the possible association between IR and ACE gene pol ymorphism 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 g lucose 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 <mu>U/mL; P < 0.001), and HOMA(IR) (2.7 +/- 1.2 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) w ere 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 muU/mL in the II group (P < 0.0001, by ANOVA). No significant differences were observed in t he normotensive control group. In conclusion, we extended previous data reg arding the relationship of hypertension and IR by demonstrating a dependenc e of this relationship upon the ACE gene polymorphism.