Fourteen case-control studies including 3371 cases and 4490 controls were recruited for the analysis of the association between ACE I/D gene polymorphism and overweight/obesity susceptibility.
The aim of this study was to establish the role of angiotensin-converting enzyme gene insertion/deletion (ACE I/D) polymorphism in determining obesity or undernutrition in a child population in Romania.
To determine the frequency of M235T and T174M-AGT, I/D-ACE and A1166C-AGTR1 in hypertensive patients with MetS and to evaluate the relationship between these polymorphisms and central obesity and dyslipidemia, respectively.
We found several synergistic effects between the studied polymorphisms and classical risk factors such as hypertension, obesity, diabetes and dyslipidaemia: the presence of the DD genotype of ACE I/D (and also ACE11860 GG) increases the odds of developing CAD when associated to each one of these classical risk factors, particularly when considering the male and early onset CAD subgroup analysis; AGT235 TT also increases the CAD risk in the presence of hypertension and dyslipidaemia, and AT1R1166 interacts positively with hypertension, smoking and obesity.
The risk of hypertension associated with ACE DD is modulated by obesity status and hence future genetic association studies should take obesity into account for the interpretation of data.
The aim of the present study was to investigate the interaction between the obesity status and ACE gene polymorphisms on the development of high level of PP.
Accordingly, nutritional composition, the content of phytochemical antioxidants, and the inhibitory ability of key enzymes with impacts on obesity and diabetes (α-glucosidase and pancreatic lipase) or on arterial pressure (angiotensin-I converting enzyme), were evaluated.
The well-known insertion/deletion polymorphism (rs4646994) of the angiotensin-converting enzyme (ACE) gene has been previously associated with obesity, blood flow, muscular strength, and ACE enzyme activity.
Subjects who carry the D allele of the angiotensin-converting enzyme (ACE) gene have higher plasma and tissue angiotensin II levels, possibly concurrent with the development of obesity.
Joint effects of hypertension, smoking, dyslipidemia and obesity and angiotensin-converting enzyme DD genotype on albuminuria in Taiwanese patients with type 2 diabetes mellitus.
We selected six single nucleotide polymorphisms (SNPs) located in angiotensin (AGT), angiotensin converting enzyme (ACE), angiotensin type 1 receptor (AGTR1), MAS1, nitric oxide synthase 3 (NOS3) and the bradykinin B2 receptor gene (BDKRB2), and genotyped them in 324 unrelated individuals with obesity (BMI ≥ 28 kg/m(2)) and 373 non-obese controls (BMI 18.5 to <24 kg/m(2)) from a large scale population-based cohort.
The prevalence of obesity according to the AACE/ACE framework was 63.1%: overweight 3.0% (95% confidence interval [CI]: 2.1-3.9); obesity stage 0: 0.1% (0.07-0.27); obesity stage 1: 26.6% (24.2-29.0); and obesity stage 2: 36.4% (33.8-39.0).
Thus, obesity is associated with the activation of renal ACE in vivo independent of its mRNA expression and enhanced vascular contractility to angiotensin II.
Our findings differ from some other previous studies using various population groups which indicate that the ACE I/D polymorphism may be differentially associated with obesity depending on multiple factors.
Similarly, the release of ACE activity in the supernatant was significantly higher in subjects with obesity with hsCRP > 3 mg/dL than in subjects with hsCRP < 3 mg/dL and controls.
Our family-based study suggests that in Chinese, the ACE I/D polymorphism might play a role in the development of obesity and hypertension, which are closely linked cardiovascular risk factors.
All the obesity and blood pressure variables were collected form 432 recruited subjects from both sexes aged 25-65 years and ACE I/D polymorphism was analysed on 299 subjects.
These findings demonstrate that the association between the ACE I/D polymorphism and obesity in relation to sodium intake is gender dependent in children.
These data suggest that obesity may alter the levels of ACE and angiotensinogen, and provide a potential pathway through which obesity leads to elevation of BP.