الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 136 |  |  |
| | | from | 136 | | |
Abstract
Non-alcoholic fatty liver disease (NAFLD) is recognized as a major public health problem in both developing and developed countries As it is the most common form of liver disease and the morbidity of which closely correlates with diversity of ethnicity, minority, family and location . It is a clinicopathologic entity with wide histological spectrum and is regarded as the leading cause of cryptogenic cirrhosis . The histologic spectrum of the disease encompasses fatty liver (simple steatosis), non-alcoholic steatohepatitis (NASH), NAFLD-associated cirrhosis and hepatocellular carcinoma (HCC).Its clinical and histological features are similar to alcohol-induced liver injury (alcoholic fatty liver disease), but it occurs in individuals without a history of excessive alcohol consumption. It is defined by the accumulation of liver fat >5% per liver weight in the presence of <10 g of daily alcohol consumption.
Adiponectin is a 247-aminoacid collagen-like polypeptide that circulates at relatively high serum concentrations (5–30 µg/ml), thereby being the most abundant and adipose-specific adipokine . Adipocytes synthesize and release adiponectin in a number of different higher-order complexes that include trimers [low-molecular-weight (LMW) form], hexamers [middle-molecular-weight (MMW) form] and 18 mers [highmolecular-weight (HMW) form though adiponectin was previously considered to be secreted exclusively by mature adipocytes .more recent studies showed that liver cells may produce adiponectin when challenged with fibrotic stimuli both in vitro and in vivo.
Clinical studies had initially shown that serum adiponectin is lower in adults and children with NAFLD than in apparently healthy controls and is inversely correlated with hepatic fat content and hepatic IR. . Serum adiponectin was also correlated with the severity of liver histology, thereby being lower in higher grades of steatosis, inflammation and fibrosis . Liver expression of adiponectin in morbidly obese patients was also decreased in patients with NASH compared with fatty liver and was associated with a higher grade of hepatic inflammation and fibrosis.
The aim of the present study is to investigate +45 T>G single nucleotide polymorphism of adiponectin gene in Non-alcoholic fatty liver disease patients.30 patients with NAFLD was subjected to complete medical history uptake and clinical examination. The demographic data of patients include : age,weight,height,blood pressure,lipid profile,liver function tests. In addition , 20 healthy ( with no evidence of acute or chronic medical disorders ).The demographic data of controls include: age, weight,height,blood pressure,lipid profile,liver function tests.
Exclusion criteria were, viral hepatitis B and C, autoimmune liver diseases, hemochromatosis, Wilson disease,choronic drug consumption and alcohol intake of more than 100g/week.
Adiponectin exon 2 +45 T>G genotyping was done by Conventional PCR .
The baseline characteristics of NAFLD patients are :-
The mean age of NAFLD patients was 47.43±11.3 5years. Majority of the patients were females (73.3%). The mean BMI of the patients was 31.93±2.58 kg/m2.all patients had BMI more than 25 kg/m2 BMI, out of which 25 patients had BMI>30 kg/m2. 36.6% of the patients had type 2 diabetes.33.3% of the patients were hypertensive. Hypertriglyceridemia and hypercholesterolemia were present in 76% and 70% of the patients, respectively.
our study shows a significant difference in the prevalence of the adiponectin gene polymorphism (+45T > G) between the case and control groups, P value (P = 0.02). Notably, the combined prevalence of the TG and TT genotypes (TG + GG), reflecting the prevalence of the T allele, was significantly greater in the NAFLD group than in the control group (P= 0.088*) with rates of 93.4% and 70%, respectively. These results imply that the T allele at position +45 in exon 2 of the adiponectin gene increases an individual’s susceptibility to NAFLD.
Also, the risk of developing NAFLD was 0.6667 times higher in patients with the TG or TT genotype (TG + TT) than in patients with the GG genotype, and this difference was statistically insignificant (95% CI: (0.11 – 3.7)
Besides, in the NAFLD group, the GG genotype was present in 2 patients, whereas the TG + TT genotypes was present in 28 patients (8+20) respectively. There were significant differences between these two groups in terms of weight (p<.05).
In addition, there were no significant differences between these two groups as regard the age ,height ,BMI ,fasting blood sugar ,blood pressure, lipid profile nor liver function tests.
Our study also showed that there were siginificant difference between the patients and controls as regard weight,BMI,blood pressure,fasting blood glucose,total cholesterol,triglycerides,HDL,LDL,AST,ALT. (p<.05).
As regard the relation between the general characteristics and each genotype,our study showed that there were significant difference between patients and controls with TT genotype as regard weight,BMI,blood pressure,fasting blood glucose,total cholesterol,LDL,triglycerides,AST and ALT.in case of GG genotype there were significant difference between patients and controls as regard weight,BMI,diastolic blood pressure and total cholesterol.patients with TG genotye differed from the controls only in the aspect of the weight.
Although we did not study the association between SNP +45 T>G and type 2 diabetes but presence of diabetes in 36.6% of the patient (p<0.01) out of which 63.3% were TT genotye ,27.2% were TG genotype and 9% were GG genotype may suggest a relation between the polymorphism and
In the present study,as regard hypertention there was significant difference between patients and controls (p=0.0178). But, no significant difference between the different genotypes of NAFLD patients (p=0.6).