OBJECTIVE: To investigate whether the genetic polymorphisms in the angiotensin I converting enzyme (ACE) (insertion/ deletion, or I/D), angiotensin II type 1 receptor (AT1R) (rs5186), and ACE2 (rs2285666) could be associated with dyslipidemia in Type 2 diabetic (T2D) patients of Chinese Han origin. DESIGN AND METHODS: The above 3 polymorphisms were genotyped in a total of 282 patients with T2D and dyslipidemia (Group A), 182 patients with T2D but without dyslipidemia (Group B), and 324 healthy controls. The association between a certain polymorphism and each group was assessed by an odds ratio (OR). RESULTS: The D allele of the ACE (I/D) was significantly associated with the risk of T2D accompanying dyslipidemia between group A and controls [OR=1.37, 95% confidence interval (CI)=1.08-1.74; p=0.010], and significant association of the D allele with dyslipidemia was also observed in diabetic patients (OR=1.88, 95% CI=1.40-2.54; p<0.001). Furthermore, the ID genotype had a decreased risk of developing T2D without dyslipidemia as compared with controls (OR=0.52, 95% CI=0.32-0.82; p=0.0060). The distributions of the AT1R (rs5186) and ACE2 (rs2285666) genotypes and alleles did not differ between T2D patients with or without dyslipidemia and the controls. CONCLUSIONS: This study demonstrates that the ACE (I/D) polymorphism is associated with T2D, regardless of the absence or presence of dyslipidemia. The polymorphisms in the AT1R (rs5186) and ACE2 (rs2285666) seem to play lesser roles in the development of T2D.
OBJECTIVE: To investigate whether the genetic polymorphisms in the angiotensin I converting enzyme (ACE) (insertion/ deletion, or I/D), angiotensin II type 1 receptor (AT1R) (rs5186), and ACE2 (rs2285666) could be associated with dyslipidemia in Type 2 diabetic (T2D) patients of Chinese Han origin. DESIGN AND METHODS: The above 3 polymorphisms were genotyped in a total of 282 patients with T2D and dyslipidemia (Group A), 182 patients with T2D but without dyslipidemia (Group B), and 324 healthy controls. The association between a certain polymorphism and each group was assessed by an odds ratio (OR). RESULTS: The D allele of the ACE (I/D) was significantly associated with the risk of T2D accompanying dyslipidemia between group A and controls [OR=1.37, 95% confidence interval (CI)=1.08-1.74; p=0.010], and significant association of the D allele with dyslipidemia was also observed in diabeticpatients (OR=1.88, 95% CI=1.40-2.54; p<0.001). Furthermore, the ID genotype had a decreased risk of developing T2D without dyslipidemia as compared with controls (OR=0.52, 95% CI=0.32-0.82; p=0.0060). The distributions of the AT1R (rs5186) and ACE2 (rs2285666) genotypes and alleles did not differ between T2Dpatients with or without dyslipidemia and the controls. CONCLUSIONS: This study demonstrates that the ACE (I/D) polymorphism is associated with T2D, regardless of the absence or presence of dyslipidemia. The polymorphisms in the AT1R (rs5186) and ACE2 (rs2285666) seem to play lesser roles in the development of T2D.
Authors: S Fröjdö; L Sjölind; M Parkkonen; V-P Mäkinen; R Kilpikari; K Pettersson-Fernholm; C Forsblom; J Fagerudd; C Tikellis; M E Cooper; M Wessman; P-H Groop Journal: Diabetologia Date: 2005-10-07 Impact factor: 10.122
Authors: Denise S Pinheiro; Rodrigo S Santos; Paulo C B Veiga Jardim; Elisangela G Silva; Angela A S Reis; Gustavo R Pedrino; Cirano J Ulhoa Journal: PLoS One Date: 2019-08-20 Impact factor: 3.240