[I/D polymorphism of angiotensin I converting enzyme gene and insulin resistance and some parameters of metabolic syndrome in patients with type 2 diabetes].
Insulinresistance is a component of the metabolic syndrome and important pathogenetic factor of type 2 diabetes mellitus. There are evidences that activation of the renin-angiotensin system (RAS) can decrease insulin sensitivity of tissues. As I/D polymorphism of angiotensin converting enzyme (ACE) gene can influence the activity of RAS, it may also influence insulin resistance. Aim. To assess the relationship between the I/D polymorphism of ACE gene and degree of insulin resistance and intensity of metabolic syndrome in type 2 diabetic patients. Study group and methods. Examined group: 108 type 2 diabetic patients (38 women and 70 men), with mean duration of disease 9.07 +/- 6.68 years, mean age 59.98 +/- 9.10 years. Assessed parameters: body mass index (BMI), waist/hip ratio (WHR), arterial blood pressure. Laboratory tests: concentration of the glycosylated hemoglobin (HbA 1c), glucose, insulin, total cholesterol, HDL and LDL cholesterol, triglycerides, creatinine, uric acid. Insulin resistance was calculated by the HOMA rate. Criterion of insulin resistance was rate > or = 2.5. The diagnosis and assessment of intensity of metabolic syndrome was performed according to criteria of National Education Cholesterol Adult Treatment Program the Panel III. I/D ACE gene polymorphism was evaluated by polymerase chain reaction (PCR). Results. Groups with 11, ID and DD genotype were not different in age, BMI, WHR, duration of diabetes, the prevalence and duration of arterial hypertension, degree of metabolic control and insulinresistance assessed by HOMA rate and intensity of metabolic syndrome. DD genotype carriers had significant higher systolic and diastolic blood pressure (147.8 +/- 19.8 mmHg vs 138.2 +/- 16.5 mmHg, p = 0,02; 89.2 +/- 9.6 mmHg vs 81.7 +/- 8.6, p = 0,003, respectively) than II patients. Conclusion. In type 2 diabetic patients the I/D genotype of ACE gene is not associated with the increased insulin resistance assessed by HOMA rate and intensity of metabolic syndrome.
Moleda
Piotr
P
Klinika Endokrynologii, Nadciśnienia Tetniczego i Chorób Przemiany Materii PAM w Szczecinie. pmoleda@wp.pl
Majkowska
Liliana
L
Safranow
Krzysztof
K
Adler
Grazyna
G
Goracy
Iwona
I
Pilarska
Krystyna
K
D000328:Adult; D000368:Aged; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000378:metabolism*; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics*; D008297:Male; D024821:Metabolic Syndrome / Q000235:genetics*; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D011110:Polymorphism, Genetic / Q000235:genetics*; D017384:Sequence Deletion / Q000235:genetics*
D007703:Peptidyl-Dipeptidase A