PCR was performed using Taq PCR Master Mix (Qiagen, Valencia, CA, USA) and T-Gradient thermal cycler (Biometra, Germany). 24 Briefly, a 109 bp fragment in the MTP gene was amplified by PCR using, the following primers: F: 5′-AGTTTCACACATAAGGACAATCATCTA-3′ and R: 5′ GGATTTAAATTTAAACTGTTAATTCATATCAC-3′ (New England Biolabs, USA). The MTP 493G/T polymorphism was genotyped by a polymerase chain reaction (PCR)-restriction fragment length polymorphism assay as described by Karpe et al. Genomic DNA was extracted and purified from whole peripheral blood samples using QIAamp DNA extraction kit (Qiagen Inc., Valencia, CA, USA). Additionally, we studied the relationship between gene variants and lipid profile of NAFLD patients with MS.

16, 17, 18, 19, 20, 2 Therefore, we performed this study to investigate whether MTP -493G > T polymorphism contributes to the risk of NAFLD and to investigate its relation with metabolic syndrome in NAFLD patients.

14, 15 The data concerning the importance of the MTP -493G > T polymorphism in NAFLD development are inconsistent. 13 Although a large number of single-nucleotide polymorphisms in the MTP gene have been identified, -493G > T (rs1800591) is one of the most common and widely investigated polymorphisms. 12 Lower hepatic expression of MTP plays a crucial role in NAFLD development. Microsomal triglyceride transfer protein (MTP, or MTTP), a lipid transfer protein involved in apolipoprotein B (apoB) assembly, is localized to the endoplasmic reticulum in hepatocytes and enterocytes. 7 Previous studies suggested that genetic factors play an important role in NAFLD etiology by altering hepatic lipid metabolism. In general, NAFLD is a multifactorial disease produced by complex interactions between nutritional factors, lifestyle choices, and genetic determinants. 5 Therefore, the possibility of NAFLD increases proportionately with the number of metabolic syndrome factors present.

4 Epidemiologic studies support belief to the relation between NAFLD and MS, the latter may be the etiologic agent that triggers the pathophysiological cascade of NAFLD.

Non-alcoholic fatty liver disease is no longer considered to be a primary liver disease, but rather a constituent of metabolic syndrome. 1 Numerous risk factors have been suggested in NAFLD pathogenesis, including advanced age, dietary habits, obesity, and some traits of metabolic syndrome (MS), such as insulin resistance and dyslipidemia. Non-alcoholic fatty liver disease (NAFLD) is a universal disorder which is considered as the most common liver disease worldwide it is defined as the accumulation of excessive fat in the liver in the absence of excessive drinking of alcohol and any secondary cause.

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