الفهرس 
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Abstract
The insulin resistance or metabolic syndrome (MS) is characterized by the clustering of metabolic abnormalities including central obesity, atherogenic dyslipidemia, hypertension and systemic insulin resistance that confer an increased risk for type 2 diabetes (DM2) and cardiovascular disease (CVD) (Després et al., 2008; Reaven, 2011; Mandavia et al., 2012).
It is generally accepted that the components of the metabolic syndrome co-exist more often than might be expected by chance (Grundy, 2006). It is also believed that central obesity and associated resistance to the metabolic actions of insulin lie at the root of the problem (Després and Lemieux, 2006; Unger and Scherer, 2010).
1.1 Insulin
Insulin is a peptide hormone, produced by beta cells of the pancreas, and is central to regulating carbohydrate and fat metabolism in the body. It causes cells in the liver, skeletal muscles, and fat tissue to absorb glucose from the blood(Sonksen and Sonksen, 2000).
The human insulin protein is composed of 51 amino acids, and has a molecular weight of 5808 Da. It is a dimer of an A-chain and a B-chain, which are linked together by disulfide bonds(Wilcox, 2005).
1.1.1 Insulin receptor
Like the receptors for other protein hormones, the receptor for insulin is embedded in the plasma membrane. The insulin receptor is composed of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha chains are entirely extracellular and house insulin binding domains, while the linked beta chains penetrate through the plasma membrane (Kido et al., 2001).
The insulin receptor is a tyrosine kinase. In other words, it functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins. Binding of insulin to the alpha subunits causes the beta subunits to phosphorylate themselves (autophosphorylation), thus activating the catalytic activity of the receptor. The activated receptor then phosphorylates a number of intracellular proteins, which in turn alters their activity, thereby generating a biological response (Kido et al., 2001)(Fig.1).