Alcoholic Steatosis in Different Strains of Rat: A Comparative Study

Abstract

BackgroundDifferent strains of rats have been used to study alcoholic liver disease (ALD) while the reason for selecting a particular rat strain was not apparent.PurposeThe aim of our study was to compare outbred (Wistar) and inbred (Fischer) strains to evaluate pathological, biochemical changes, and gene expression differences associated with ethanol-induced early hepatic steatosis.Study DesignMale Wistar and Fischer-344 rats were pair-fed for 6 weeks with or without 5% ethanol in Lieber-DeCarli liquid diet. Livers were analyzed for histological and lipid-related differences.ResultsHepatic midzonal steatosis was mainly found in Wistar rats while Fischer rats showed mostly pericentral steatosis. Increased hepatic steatosis in ethanol-fed Wistar rats is supported by increases in lipids with related genes and transcription factors involved in fatty acid and triglyceride synthesis.ConclusionOur data showed that Fischer rats are relatively less prone to ethanol-mediated steatosis with pericentral lipid deposition pattern in the liver which is similar to humans and show no trace level of lipid accumulation in pair-fed controls as observed in Wistar (outbred) strain. Therefore, Fischer rats are better suited for lipid studies in an early development of ALD.

Resveratrol improves alcoholic fatty liver disease by downregulating HIF-1α expression and mitochondrial ROS production

“…TG content in liver was determined as previously described [ 19 ]. Briefly, 250 mg of liver sample was homogenized in 1.5 mL of methanol, and then added with 5.0 ml of MTBE and shaken at room temperature for 1 h. Subsequently, 1.25 mL of high purity water was added and mixed for 10 min, followed by centrifuging at 1,000 g for 10 min, and the upper organic layer was collected.…”

Alcohol-Induced Hepatic Steatosis: A Comparative Study to Identify Possible Indicator(s) of Alcoholic Fatty Liver Disease

“…Animal experimentation was performed in accordance with the protocol approved by Institutional Animal Care and Use Committee of the University of Texas Medical Branch, USA, and followed the NIH Guidelines for care and use of laboratory animals. Rats were housed in humidity and temperature-controlled animal room with automatic 12h light/dark cycles and the experiment was carried out as described previously [13,14,15,16]. After 1 week of acclimatization, rats were divided into three groups (6–7 animals in each group).…”

“…The liver from each animal was harvested, grossly examined and weighed. Two small sections of the liver from the left lobe were cut, one frozen in liquid nitrogen and the other stored in 10% buffered formalin for tissue section cutting and hematoxylin and eosin (H&E) staining and the remaining parts of the liver stored at −80 0 C. The steatosis was graded by histological examination for accumulation of fat in the hepatocytes and confirmed by Oil Red ‘O’ staining for lipid deposition as described earlier in [16, 18].…”

“…The plasma samples were analyzed for hepatic injury markers using alanine aminotransferase (ALT/SGPT Liq-UV), alkaline phosphatase (ALP Liquicolor) and lactic dehydrogenase (LDH-Liq-UV) kits from Stainbio Laboratory, Boerne, TX, USA and aspartate aminotransferase (AST/SGOT) reagent kit from TECO diagnostics, Anaheim, CA,USA as used previously [16].…”

“…Thus differential distributions of lipids as a result of diet, ethanol or other factors are important in the etiopathogenesis of alcoholic fatty liver. In our previous work, we studied hepatic lipid profiling after ethanol feeding in rats and mice under various scenarios [13,14,15,16]. The altered lipids were found to be cholesterol, fatty acids, phospholipids and triglycerides when LD group was compared with LED group.…”