Abstract

We studied angiotensin-converting enzyme (ACE) gene polymorphism and lipid profiles in Kuwaiti children with uncomplicated type 1 diabetes. A total of 125 children with type 1 diabetes were matched in a case-control study on age and gender to 125 non-diabetic children as controls. Serum lipids (total cholesterol, TC; high-density lipoprotein cholesterol, HDL; low-density lipoprotein cholesterol, LDL-c; triglycerides, TG; apolipoprotein A1 and B, apo A1 and B; lipoprotein(a), Lp(a)); and glycated hemoglobin, HbA1c were evaluated according to ACE genotypes. Genotype distributions were found to be similar in cases [ACE insertion/insertion (II) 9.6%, ACE insertion/deletion (ID) 38.4%, ACE deletion/deletion (DD) 52.0%], and controls (II 8.8%, ID 43.2%, DD 48.0%), and were characterized by higher frequencies of DD, ID, and lower frequencies of II. Diabetic children with DD genotype showed significantly higher levels of TC (p < 0.01), HDL (p < 0.001), and apo A1 (p < 0.001) than controls. There was a higher proportion of diabetic children with family history of cardiovascular disease (CVD) in the DD genotype group (51.9%) than those with II genotype group (11.1%) (p < 0.001). Also, there was a significant increase in the frequency of diabetic children with Lp(a) > 30 mg/dL in children with a family history of CVD (p = 0.008). Lp(a) levels were correlated with HbA1c in the diabetic group (r = 0.239, p = 0.019), but when patients with poor glycemic control (HbA1c > 9%) were excluded, the significant correlation disappeared (r = 0.127, p = 0.381). After adjusting confounding between variables, the logistic regression analysis showed that the two significantly related variables with the rise in Lp(a) were increasing TC level and poor glycemic control. In children with type 1 diabetes, the role of ACE polymorphism as a probable contributor to CVD seems to be partially mediated through other factors such as poor glycemic control, TC, and Lp(a) level. A longitudinal study is recommended with a larger number of patients in each ACE genotype group in order to assess such associations.

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