الفهرس 
OBESITYOnly 14 pages are availabe for public view
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Abstract
A dipose tissue known to be an endocrine organ does not only store energy but also secretes many hormones and cytokines, collectively named as adipocytokines. Visfatin is a recently described adipocytokine that was identified in 2005. It is predominantly found in visceral fat, however, it can also be found in skeletal muscle, liver, bone marrow, and lymphocytes. Visfatin, initially identified as a pre–B-cell colony-enhancing factor, functions as an immunomodulatory cytokine and is involved in the regulation of inflammatory responses. In addition, visfatin helps in the regulation of glucose homeostasis, actually exhibited insulin mimetic properties resulting in a glucose-lowering effect. Furthermore, visfatin promotes the storage of triglycerides in preadipocytes and stimulates adipogenesis. Current data are suggestive of a role of visfatin in lipid homeostasis (Catalán et al., 2011).
The aim of the present study was to assess serum visfatin level as well as its relation to selected anthropometric and biochemical parameters in adult obesity. The study was conducted on 44 morbidly obese subjects and 44 age and sex matched individuals as a control group. All subjects enrolled were subjected to full history taking, clinical examination, assessment of anthropometric parameters (BW, BMI, WC and HC) as well as biochemical parameters (serum total cholesterol, triglycrides, FBG and fasting insulin). Insulin resistance was assessed by HOMA-IR. In addition, serum visfatin was assessed using commercially applied ELISA kit.
The study demonstrated that morbid obese subjects had significantly higher serum visfatin levels than lean individuals. As regarding relations of visfatin to anthropometric parameters, we have found a significant positive correlation between visfatin and each of BMI and WC in obese subjects, as well as between serum visfatin and HC. Moreover, we have also observed that fasting insulin and HOMA-IR were significantly higher among obese individuals than controls. However, a significant difference in fasting blood sugar levels was not observed between the two studied groups.
On the other hand, significant differences in the levels of triglycerides and total cholesterol between obese and non obese subjects have been observed in the present study. However, no significant correlations were obtained between both parameters and visfatin neither in control nor in obese individuals.
In conclusion, the observed significant elevation of visfatin together with its significant correlation to HOMA index in obesity is suggestive of a role of visfatin in glycemic control. Further studies are required to better define the possible role of visfatin in glucose homeostasis and whether it is also involved in lipid homeostasis.