الفهرس 
nsulin resistanceOnly 14 pages are availabe for public view
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Abstract
I
nsulin resistance is defined as reduced sensitivity of target organs to the biologic effects of insulin. Major functions of insulin include stimulation of glucose uptake by skeletal muscles, inhibition of hepatic glucose production, and inhibition of lipolysis in adipose tissues (Stumvoll et al., 2005).
Insulin resistance has been associated with increased risk of cardiovascular events and mortality in multiple large community-based cohort studies (Shinohara et al., 2002).
Insulin resistance is common in end-stage renal disease (ESRD), and possibly also in moderate-to severe stages of CKD. Therefore, insulin resistance may be an important therapeutic target for reduction of cardiovascular mortality in patients with CKD (Siew and Ikizler, 2010).
Causes of insulin resistance in CKD include various uremic toxins, metabolic acidosis, and vitamin D deficiency. Asymmetric dimethyl arginine (ADMA) has been increasingly recognized as an important uremic toxin associated with CKD and insulin resistance. It is an endogenous inhibitor of nitric oxide production and is an important mediator of endothelial dysfunction (Kielstein and Zoccali, 2005).
In recent years, adipose tissue has been found to be a major source of many proteins that may directly contribute to vascular injury, diabetes, and atherogenesis (Raiala and Scherer, 2003). These proinflammatory adipokines include TNF-α, IL-6, leptin, plasminogen activator inhibitor-1, angiotensinogen, and resistin, among many others. In contrast, the adipokine adiponectin confers protection against inflammation, atherogenesis, and obesity-linked insulin resistance.
A recent addition to the now formidable list of contenders as a pivotal factor in mediating obesity-driven diabetes is retinol binding protein 4 (RBP4). RBP4 has been proposed to be a marker for diabetes and also potentially a target for therapy (Raiala and Schere, 2003).
Retinol-binding protein 4 (RBP4) is a 21 kDa non-glycosylated, non-phosphorylated, and non-sulfated molecule (Jaconi et al., 1995)
It is a lipocalin superfamily molecule (Blomhoff et al., 1992) that is synthesized primarily by hepatocytes and adipocytes. This liver-derived transport protein retinol-binding protein (RBP) has recently been proposed as a novel adipokine involved in the metabolism of glucose (Axelsson et al., 2009).
Elevated plasma levels of the insulin resistance–associated adipokines RBP4 and resistin was reported in CKD patients (Yaturu et al., 2007)
This study was conducted on 100 individuals divided into two groups of comparable age and sex as follows:
group I: Patients group consist of 50 ESRD patients on regular hemodialysis; they were 20 females (40.0%) and 30 males (60.0%) with mean age ±SD (38.08±7.1 years).
group II: 50 healthy individuals as a control group; 26 females (52%) and 24 males (48%) with mean age ±SD (35.38±8.77 years).
According to insulin resistance (HOMA level) each group will be subdivided into two subgroups:
Subgroup (A) when HOMA<2.
Subgroup (B) when HOMA ≥2.
There was a highly significant increase in RBP4 (p 0.000) and FBG (0.005) in hemodialysis patients compared control group. There was statistically significant increase in FBI in hemodialysis group compared to control group (p 0.043), while there was no statistically significant difference found between the two studied groups regarding HOMA and 2h post challenge blood glucose (p 0.260).