الفهرس 
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Abstract
Twenty adult male albino rats with average weight 250300g were used in this study. The animals were divided into four groups (five animals each). Group (I): were orally fed with high fat diet as corn oil (25% of calories). Group (II): were orally fed with high fat diet plus gradual increase of ethanol concentration until it reached 49% for 16 weeks.
Group (III): were orally fed with high fat diet plus increasing ethanol concentration until it reached 49% plus iron sucrose (Ferosac, Novartis Pharmaceutical). Iron was given orally (0.25% wt/vol) twice per day and injected intramuscularly twice per week for 16 weeks at a dose of 0.4mg/g/day. Group (IV): is the control group fed with standard rat diet. The control animals had free access to food and water. Sixteen weeks after the beginning of the experiment, rats were sacrificed. The sections were cut at 5 and subjected to the following stains: hematoxylin and eosin stain for histopatholgical changes of the liver, McFarlane trichrome, silver reticulin and sirus red stains to detect the degree of fibrosis, Perls Prussian blue stain to detect hemosidrosis of the liver and ga ssmooth muscle actin immunoperoxidase stain was used to detect activated stellate cells. Aim of the work The aim of the work is to study the effect of high fat diet composition on the liver and the role of dietary iron supplementation in exacerbation of alcoholic liver fibrosis. Results In the control group, macroscopic and histological examination revealed normal appearance of the liver cells. Group I (high fat diet), hepatic steatosis (panacinar, macrovesicular) which was complicated by the presence of Mallory bodies. Morphometric measurements of the area and area% of amount of fibrosis were higher compared to that of control group Group II (high fat and alcohol), hepatic steatosis (panacinar macrovesicular and microvesicular) there were perivenular, portal and periportal fibrosis with bile duct proliferation. Sections stained with Perls Prussian blue stain, showed hemosidrin pigment deposition in kupffer cells. In sections stained with ga ssmooth muscle actin immunoperoxidase stain, there was increase in the number of stellate cells. Morphometric measurements of the area and area% of amount of fibrosis were increased compared to that of control and group I. Group III (high fat, alcohol and iron), piecemeal necrosis infiltrated by inflammatory cells were seen. In sections stained with McFarlane trichrome, silver reticulin and sirus red stains, there were perivenular, portal, periportal and portoportal bridging fibrosis with capillarization of sinusoidal wall. Psudo micronodular cirrhosis was detected in one animal which appeared as two circumscribed lesions connected by thick band of fibrous tissue. Sections stained with Perls Prussian blue stain showed moderate diffuse hemosidrin pigment deposition in kupffer cells and in the cytoplasm of the hepatocytes. Sections stained with ga ssmooth muscle actin immunoperoxidase stain showed positive stellate cells. ga ssmooth muscle actin positive cell could be seen around portal tract and in the wall of bile duct. Morphometric measurements of the area and area% of the amount of fibrosis were increased compared to that of the control, group I and group II Summary and Conclusion In conclusion, nonalcoholic fatty liver is highly associated with high fat diet and obesity which produce hepatic steatosis and may be complicated by inflammation (steatohepatitis, NASH). Alcohol ingestion associated with high fat diet promote steatosis which become high enough to injure liver and progress to fibrosis. In the present study, excess iron in alcoholinduced liver damage and alcohol excess in ironoverload disease are powerful cocktails promoting subcellular organelle damage leading to cell death and fibrosis and cirrhosis.