الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Non-alcoholic fatty liver disease (NAFLD) refers to a condition defined by ectopic fat accumulation in the form of triacylglycride (TG) in the liver, when it accounts for more than 5 % of the total organ weight, in the absence of secondary causes The major risk factors for NAFLD are the same as the components of the metabolic syndrome (MS), Today, NAFLD is considered to be the hepatic component of the MS. The clinical spectrum of NAFLD ranges from simple fatty change to nonalcoholic steatohepatitis (NASH).
The homeostasis of fat and energy in hepatic cells is regulated by mitochondrial activities, including beta-oxidation of free fatty acids (FFAs), electron transfer and production of adenosine triphosphate (ATP), and reactive oxygen species (ROS). Mitochondrial abnormalities leading to the blockade of fatty acid beta-oxidation and the consequent induction of ROS production.
ROS and other products of lipid peroxidation impair the respiratory chain in hepatocytes which is also an important subcellular source of ROS. Impaired oxidative phosphorylation resulting in reduced hepatic ATP synthesis and increased ROS production has been reported in patients with NASH.
Sirtuins (SIRT) are a class of proteins that possess either mono-ADP-ribosyltransferase, or deacylase activity, including deacetylase, desuccinylase, demalonylase, demyristoylase and depalmitoylase activity. Sirtuins have been implicated in influencing a wide range of cellular processes and physiological functions including hepatic glucose and fatty acid metabolism, mitochondrial function.
Previous studies have shown that SIRT1 decreases hepatic TAG levels by inhibiting lipogenesis and stimulating fatty acid β-oxidation. Activation of SIRT1 could serve as an effective therapeutic approach for preventing the development of fatty liver diseases at all stages, including the onset, progression and complication. Resveratrol was identified as direct SIRT1 activator for the first time.
It is known that vitamin D deficiency and NAFLD, are linked to obesity and a sedentary lifestyle both directly and indirectly, therefore, lack of vitamin D exists simultaneously with NAFLD. The linking vitamin D3 to NAFLD is still not fully understood, but previous studies on animals showed that vitamin D plays an important role in regulating OS, pro-inflammatory cytokine production, apoptosis of hepatocytes and even liver fibrosis.
This study was carried out on 40 male Wistar albino rats with body weight 150-200 grams, the duration of this study was 16 weeks for all groups. Rats were divided randomly into 4 experimental groups, each of it included ten rats:
group 1 (control group): fed on standard rat chow containing carbohydrates 51%, protein 16%, vitamins and minerals 4%, and lipids 3%, the standard diet contained 2.9 Kcal per 1g of diet.
group 2 (NAFLD group): fed on high-fat chow from the first week, containing carbohydrate 24.55%, protein 14.47%, fat 60.98%, presenting a total of 5.28 Kcal per 1 g of diet, for 16 week.