Key result
ACE I/D polymorphisms were not associated with T2DM or MetS in 516 Jordanians, though ID and II genotypes increased odds of hypertension and microalbuminuria.
Why the study?
Metabolic syndrome significantly increases the risk of cardiovascular disease and Type 2 diabetes mellitus, prompting an evaluation of the association of angiotensin converting enzyme insertion/deletion polymorphisms with these conditions in a Jordanian population.
Are angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphisms associated with metabolic syndrome and Type 2 diabetes mellitus in a Jordanian population?
Case-Control (n=516)
Are angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphisms associated with metabolic syndrome and Type 2 diabetes mellitus in a Jordanian population?
In a Jordanian cohort, ACE I/D gene polymorphisms were not associated with overall susceptibility to Type 2 diabetes or metabolic syndrome, but specific genotypes were linked to the clinical endpoints of hypertension and microalbuminuria.
Metabolic syndrome (MetS) is consisted of central obesity, raised blood pressure, insulin resistance, and dyslipidemia, it significantly increases the risk of cardiovascular disease and Type 2 diabetes mellitus (T2DM). MetS prevalence globally is estimated to be between 14% to 32% making MetS a significant a critical public health. The aim of this study was to check the association of angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphisms with Type 2 diabetes mellitus (T2DM) and MetS a Jordanian population by a case-control study design. The total participants included 516, 148 and 127 patients with T2DMand MetS, respectively, and 241 healthy control. The I/D polymorphisms of ACE were determined by polymerase chain reaction (PCR) technique. In biochemical analysis, levels of lipid panel, fasting plasma glucose, glycated hemoglobin (HbA1c), and activity of plasma ACE were measured. Enzyme-linked immunosorbent assay (ELISA) was used to quantify levels of apolipoprotein A1 and plasma insulin, urinary microalbuminuria was assessed via semi-quantitative test strips. Overall the distribution of ACE genotypes was not different or the allele frequencies between the study groups. Analysis of clinical outcome, on the other hand revealed that ACE ID polymorphism was significantly associated with increased odds of hypertension, while II polymorphism and I allele were associated with increased odds of microalbuminuria. Conversely, DD genotype showed a significant negative association with both hypertension and microalbuminuria, which might be a protective effect. These data suggest that ACE I/D polymorphisms were not significantly linked to the susceptibility to T2DM or MetS in this population, but may be associated with certain clinical end points of these diseases. Additional research should be made in larger, ethnically diverse groups of participants to confirm these associations.
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Mahgoub et al. (2026) conducted a case-control in Type 2 diabetes mellitus and metabolic syndrome (n=516). ACE gene insertion/deletion (I/D) polymorphisms vs. Healthy controls (n=241) was evaluated on Association of ACE I/D genotypes and allele frequencies with Type 2 diabetes mellitus and metabolic syndrome. ACE I/D polymorphisms were not associated with T2DM or MetS in 516 Jordanians, though ID and II genotypes increased odds of hypertension and microalbuminuria.
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