الفهرس 
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Abstract
Metabolic syndrome (MS), is defined by the clustering of several cardiovascular risk factors in an individual patient, including type II diabetes, hypertension, dyslipidemia, and central obesity. A participant in our study has the metabolic syndrome if he or she has impaired fasting glucose or diabetes plus two or more of the following components: 1) raised arterial pressure ≥140/90 mmHg or on antihypertensive treatment; 2) central obesity (WHR > 0.9 for men and > 0.85 for women and/or BMI > 30 kg/m2); 3) microalbuminurea (urinary albumin excretion rate ≥ 20 µg/min or albumin/creatinine ≥ 20 mg/g on at least two different occasions) or more advanced nephropathy; and 4) raised plasma triglycerides (≥150 mg/dl) and/or decreased HDL cholesterol (< 35 mg/dl for men; < 39 mg/dl for women).
Studies on the genes have proposed the renin-angiotensin system (RAS) as an important genetic factor for diabetic complications. One of the RAS genes is gene coding the angiotensin converting enzyme (ACE). The polymorphism consists of the presence (I allele) or absence (D allele) of a 287 bp. Activated angiotensin systems through insulin resistant may lead to organ damage by enhancement of cellular hypertrophy and proliferation and disruption of the extracellular matrix, and induction of cytokine or growth factor secretion further exacerbates the injury.
The aim of this work is to study the association of ACE activity and genotyping with metabolic syndrome, and to try to asses the possible role of ACE genotyping in the pathogenesis of varying components of metabolic syndrome.
This study was carried out in the medical Biochemistry and Internal Medicine Departments, Faculty of Medicine, Zagazig University.
Eighty subjects were included and were classified into 3 groups:
Control group: Comprising 20 healthy subjects (9 males and 11 females; with a mean age of 53.5 4.8 years) not suffering from any disease interfering with our study.
Type II diabetes group: Comprised 20 subjects (12 males and 8 females; with a mean age of 56.15.8 years) with type 2 diabetes and without any other component of metabolic syndrome.
Metabolic group: Comprised 40 patients (17 males and 23 females; with a mean age of 54.94.6 years) with type 2 diabetes and two or more of other components of metabolic syndrome.
All groups well further subclassified according to genotype (DD, ID, II).
Research investigations:
- Determination of ACE genotypes by PCR amplification
- The ACE activity was determined by a colorimetric method
- Determination of fasting blood glucose by enzymatic method
- Estimation of glycohemoglobin (HbA1c) in blood
- Measurement of fasting insulin by ELISA
- Determination of insulin resistance by Homeostasis model assessment (HOMA) index calculated by the following formula: HOMA index = [fasting insulin (µU/ml) x fasting plasma glucose (mmol/l)] / 22.5. Subjects were considered to have insulin resistance if HOMA was greater than 1.64
- Detection of microalbuminuria by dipstick method.