الفهرس 
OBESITYOnly 14 pages are availabe for public view
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Abstract
O
besity is a complex chronic disorder with a multifactorial etiology, involving genetics, hormones, diets, and environments (Kollias and Sfikakis, 2010).
The World Health Organization (WHO) has reported that obesity has been growing at an alarming rate, accounting for approximately 35% of the population. This proportion has consistently increased over the last decade and the rates of type 2 diabetes have increased markedly over the last 50 years in parallel with obesity (Smyth and Heron, 2006).
Recent work in the area of Obesity has confirmed that Obesity is a state of low grade chronic inflammation and is associated with increased levels of Tumor Necrosis Factor-α, a pro-inflammatory adipocytokine, which plays a key role in the pathogenesis of obesity and diabetes (Rajarajeswari et al., 2011).
This thesis was carried out to determine the serum level of tumor necrosis factor α (TNF-α) in obese non diabetic and obese type 2 diabetic patients (NIDDM) and its relation to insulin level and to clinical assessment of obesity.
We conducted our study on 40 obese patients in addition to 10 lean persons who are serving as a control group.
The patients were divided into 2 groups. Group I included twenty obese non diabetic patients and group II included twenty obese patients newly diagnosed with type2 diabetes.
All patients were subjected to complete history taking, thorough clinical examination, measuring serum TNF-α, insulin and measuring insulin resistance using Homeostasis Model of Assessment (HOMA-IR) and calculation of body fat percentage using skin fold thickness summation.
Our study revealed significant positive correlation between TNF-α and BMI. TNF-α levels were significantly elevated in obese diabetic than obese non diabetic and control subjects. And that suggest a possible role of TNF-α in the pathophysiology of Type2 diabetes.
Our study revealed highly significant positive correlations between serum TNF-α level and WC and HC in both groups as indices of obesity but no correlations was found between TNF-α level and WHR in group II.
Our study revealed significant positive correlation between TNF-α and body fat percentage that indicate that serum TNF-α is correlated to the degree of adiposity with the fact that TNF-α not only secreted from adipocytes, but also from macrophages in white adipose tissue.
We conclude that TNF-α may play a potentially important pathophysiological role in the development of insulin resistance in people with high BMI as we found correlation between TNF-α and insulin level and HOMA.IR in obese non diabetic and was not found in obese diabetic group that indicate the compensatory over functioning of beta cells to release insulin to nullify the insulin resistance produced by TNF-α in the peripheral tissues caused by obesity and prove that the TNF-α increased before the onset of diabetes and further increase was not associated with insulin resistance. So TNF-α can be used as risk indicator for the future development of type2 diabetes.
We also prove that TNF-α expression is not tightly linked to differences in distribution of body fat as we found no correlation between TNF-α and WHR in obese diabetic patients but related to the total degree of adiposity.