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Angiotensin‐converting enzyme gene polymorphism and lipid profiles in Kuwaiti children with type 1 diabetes
Author(s) -
Alsaeid M.,
Moussa M. A. A.,
Haider M. Z.,
Refai T. M. K.,
Abdella N.,
AlSheikh N.,
Gomez J. E.
Publication year - 2004
Publication title -
pediatric diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.678
H-Index - 75
eISSN - 1399-5448
pISSN - 1399-543X
DOI - 10.1111/j.1399-543x.2004.00040.x
Subject(s) - medicine , endocrinology , genotype , angiotensin converting enzyme , diabetes mellitus , glycemic , glycated hemoglobin , apolipoprotein b , type 2 diabetes , lipid profile , polymorphism (computer science) , lipoprotein , cholesterol , gene , biology , genetics , blood pressure
Methods: 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. Results: 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. Conclusions: 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.