الفهرس 
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Abstract
Resistin was discovered in 2001 by the group of dr. Mitchell A. lazar from the university of Pennsylvania school of medicine. It was called ”resistin” because of the observed insulin resistance in mice injected with resistin. Resistin is a cysteine-rich, 108 – amino – acid peptide hormones with a molecular weight of 12.5 KDa, that in humans, it is encoded by the RETN gene.
Insulin resistance is a prediabetic stage, so type2 diabetes mellitus could be regarded as a disease where the islet adaptation to insulin resistance fails.
It is currently established that central obesity is a contributing factor to the pathogenesis of insulin resistance and consequently to T2DM. Although it is apparent that inconsistencies remain in the data for a role of resistin in obesity, there is a growing body of evidence suggesting a role for resistin in the etiology of insulin resistance and T2DM.
The aim of our stydy is to investigate the correlation between serum resistin level and insulin restance in obesity and type 2 diabetes mellitus together with serum resistion to the severity of diabetic microangiopathy.
This study was carried out on 50subjects (five groups), classified (according to BMI, presence of type2 DM and diabetic retinopathy) as below:
GROUP 1:comprised 10 non obese non diabetic (healthy volunteers). With a mean (BMI) of 21 1.6 kg /m2. They were 4 males and 6 females, their ages range from 30 to 55 years (mean 43 years).
GROUP 2: COMPRISED 10 OBESE, NON DIABETIC SUBJECTS. WITH A MEAN (BMI) of 33.1 +- 1.4 kg/m2. They wree 6 males and 4 females, their ages range from 31 to 52 years (mean 40.6 years).
GROUP 3 : this group consisting of thirty obese, diabetic patients they were subjected to fundus examination , then divided into 3 subgroups:-
GROP 3 A: This group consists of ten diabetic patients with no clinical evidence or fundus examination suggestive of retinopathy. With a mean (BMI) of 36.00 +- 4.2 kg/ m2. THEY WERE 5 MALES AND 5 FEMALES; their ages range from 43 to 71 years (mean 54.6 years).
GROUP 3 B : This group consists of ten diabetic patients with non proliferative diabetic retinopathy, with a mean (BMI) OF 36.50 +- 6.5 KG/M2. They were 2 males and 8 females ; their ages range from 52 to 72 years (mean 59.8 years).
GROUP 3 c : including ten patients with proliferative diabetic retinopathy, with a man (BMI) of 33.9 +- 2.4 kg/m2. They were 4 males and 6 females; their ages range from 54 to 70 years (mean 56.4years).
Patients were referred from the Department of Ophthalmology, Benha University Hospital, and Benha Ophthalmology Hospital. Blood samples were collected and subjected to the following investigations:
• Fasting bloodglucose level.
• Fasting serum insulin level
• Fasting resistance measurement.
• Serum C- REACTIVE PROTEN.
• Lipid profile.
• Serum resistin level by ELISA.
The biochemical study was done in the department of Biochemistry, faculty of Medicine, Benha University.
Our results showed that fasting glucose and insulin resistance, as assessed using the homeostasis model of insulin resistance ratio (HOMA-R), were similar in non obese and obese subjects.
Fasting serum restin was highly significantly (P<0.0001)different among the five groups (tablel) mean serum resistin concentration increased from non obese and obese diabetic to diabetic non retinopathy subjects to subjects with non-proliferative diabetic retinopathy to subjects with proliferative diabetic retinopathy. Bon ferroni adjustment revealed that there was significant difference between diabetic non retinopathy subjects and subjects with proliferative diabetic retinopathy.
Fasting serum resistin concentrations were not correlated with LDL cholesterol whereas there was a highiy significant positive correlation between serum resistin and triglycerides, CRP, BMI, serum insulin, I.R, FBS. Serum resistin is significantly positively correlated with wasist and hip circumferences while it was significantly negatively correlated with HDL cholesterol.