الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Dyslipidemia is one of the key risk factors for cardiovascular disease in diabetes mellitus. The characteristic features of diabetic dyslipidemia are high plasma triglyceride concentration, reduced high density lipoprotein cholesterol concentration, and increased concentration of small dense low density lipoproteinparticles. These lipid derangements are intrinsically related to the abnormal physiology produced by insulin resistance. A main cause of the elevated TG concentration is overproduction of VLDL in the liver, provoked by an increased flow of free fatty acids (FFA) to the liver. Additionally, there may be reduced catabolism ofthe triglyceride rich lipoproteins (VLDL and chylomicrons), due to reduced activity of lipoprotein lipase (LPL) which is controlled by insulin.Achievement of recommended lipid and lipoprotein targets usually requires pharmacological and non-pharmacological therapy. The non- pharmacological approaches include dietary modification which is an important component in the management of dyslipidemia.Increased physical activity that can improve insulin sensitivity and increase HDL-C levels.
The major goal of lipid-modifying therapy in most patients with disorders of lipid metabolism is to prevent CVD and its complications.
A number of pharmacological agents are available which help patients to attain the recommended LDL-C levels which include 3-hydroxy3-methylglutarylcoenzyme-A reductase (HMGCoA-R) inhibitors (statins), fibric acid derivatives, bile acid sequestrants,niacin,ezetimibe,omega-3 fatty acids are proven to be lifesaving medications.
Statins are competitive and reversible inhibitors of 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCoAreductase), the rate-limiting enzyme for cholesterol synthesis. By this mechanism, statin medication effectively reduces intracellular cholesterol levels by activating several genes such as the low-density lipoprotein receptor (LDLR).However, there is, substantial inter-individual variation in the magnitude of statin-induced LDL-C reduction, that has been attributed to both phenotypic and genetic factors. Phenotypic predictors include age, ancestry and smoking status. However the genetic factor in the form of polymorphism in genes affecting statin pharmacodynamics and pharmacokinetics, such as HMG-CoA-R, ApoE, and LDLR.
In the present study we follow up a 96 diabetic Egyptian patients for three months and they received Atorvastatin 20 mg /day. The lipid profile was assessed at base line and after follow up period of three months and according to change in LDL –C level the participants were divided into responder and non-responder groups. Genotyping was performed to assess the presence of SNP rs 12916 C/T which occur in HMGCoAreductaseenzyme. Phenotypic factors s