الفهرس 
OBESITYOnly 14 pages are availabe for public view
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Abstract
Obesity is a worldwide epidemic that continues to grow at an alarming rate. Some of the deleterious consequences of obesity have been attributed to its induction of a low-grade chronic inflammatory state that arises from the production and secretion of inflammatory mediators from the expanded pool of activated adipocytes.
White adipose tissue was believed to be just an energy storage organ but now it is recognized to be an active participant in energy homeostasis and physiological functions such as immunity and inflammation. Adipose tissue is known to secrete and express a variety of products known as adipokines including leptin, adiponectin, resistin and visfatin as well as cytokines and chemokines such as TNF-α, IL-6 and MCP-1. The release of adipokines by either adipocytes or adipose tissue-infiltrated macrophages leads to a chronic sub-inflammatory state that could play a central role in the development of insulin resistance and type 2 diabetes, and the increased risk of cardiovascular disease associated with obesity.
It was reported that, there are three scenarios have been proposed to explain the relation of obesity to the insulin resistance. The first scenario is the hyperlipolytic state of the omental adipose tissue. The second scenario is proinflammatory cytokines that are produced by adipose tissue. The third scenario is the relative inability of subcutaneous adipose tissue to act as a protective metabolic sink because of its inability to expand or because it has become hypertrophied, dysfunctional and insulin resistant.
Resistin is a 10 kDa protein of 94 amino acids, which belongs to a cysteine-rich protein family and was cloned in 2001 as a thiazolidinediones (TZD)-regulated cytokine expressed in adipose tissue. Its effects on insulin action have been extensively investigated in mice, where resistin is involved in hepatic glucose and lipid metabolism and appears to be a major determinant of hepatic insulin resistance induced by high-fat diet. It reduces insulin sensitivity in adipocytes and skeletal muscles by impairing insulin-mediated glucose transport and inducing the expression of suppressor of cytokine signaling 3 (SOCS3), and regulates fasting blood glucose by increasing hepatic glucose release.
In humans it is produced by macrophages as well as adipocytes. It exerts a variety of effects on endothelial and immune cells that are consistent with an inflammatory mediator. Resistin is associated with an increased production of pro-inflammatory cytokines and a decreased production of anti-inflammatory cytokines, with the former mediated through NFkB activation. Macrophages also respond to resistin stimulation by producing pro-inflammatory cytokines such as TNF-a, IL-12, and IL-6. Also resistin levels appear to correlate with other inflammatory markers, such as C-reactive protein (CRP), in different pathological conditions.
The present study was undertaken aiming to evaluate the effect of obesity as a process of low grade of inflammation on the concentration of resistin. The study also aimed to assess the correlation between resistin on one side and the insulin resistance and hs-CRP as an inflammatory marker on the other side.
Two groups of individuals were included in the study patients group, including 53 morbidly obese individuals with BMI ≥40 kg/m2 this group was further subdivided into 2 groups ’’obese diabetic group and obese non-diabetic group” and control group that included 30 age and sex matched normal weight controls with mean BMI ≤24.9kg/m2. Quantitative assays of serum resistin and hs-CRP, using commercially supplied ELISA were performed for all individuals. In addition to, the assessment of fasting insulin, fasting blood sugar and lipid profile for both groups.
Statistically high significant differences as regards serum levels of resistin and hs-CRP were found between the 2 studied groups; patients group had higher levels. Additionally, correlation studies have revealed significant positive correlations between resistin and each of hs-CRP, insulin and HOMA-IR among obese diabetic individuals and highly significant correlation between resistin and each of hs-CRP and total cholesterol in obese non diabetic group.
In Conclusion, we have shown that high levels of resistin are associated with an increased risk of insulin resistance, and that resistin might be a stronger predictor of insulin resistance and diabetes in persons who are considered at lower risk of diabetes as lean individuals.