Hepatic histologic findings in a murine model of diet induced-steatotic liver disease and acute alcohol intake

Abstract

Introduction and Objectives: Steatotic liver disease is produced by a range of etiologic agents, among them metabolic and alcoholic. Our aim was to identify the histologic findings produced in the liver after the interaction of steatosis induced by the methione-choline deficient (MCD) diet and the acute ethanol consumption in a murine model. Materials and Patients: 46 male, 10 week-old, C57BL/6 mice were randomly assigned to the following groups: Control, fed LabDiet 5010; MCD, fed the steatogenic diet MCD for 6 weeks; OHa, fed LabDiet, this group received 8 doses i.p. of ethanol (2.5g/Kg), within a scheme of 2 days of administration followed by 1 day rest; MCDOHa, fed MCD for 6 weeks, this group receive 8 ethanol doses during weeks 5 and 6, as described earlier; a group receiving vehicle with the same scheme as the ethanol was included. After treatments, livers were collected. Paraffin sections were stained with hematoxylin-eosin and Masson's thrichrome. Samples were analyzed. Representative histologic findings were considered when present in at least 50% of the samples per group. Results: Control and vehicle livers did not show alterations. MCD livers showed macrovesicular steatosis (range 33-66%) in portal and central areas, with few or non ballooning, inflammation was observed, as well as portal fibrosis (F1C). OHa group did not showed steatosis, 57% of samples showed sinusoidal dilation in portal areas; necrosis and inflammation were also observed in the portal triad. Fibrosis was observed in 50% of livers. Interaction of both stimulus (MCDOHa) produced macrovesicular diffused steatosis ranging from 50-90% of liver area. 56% of samples showed few ballooning. Increased inflammatory foci were observed compared with MCD. Regarding fibrosis, 56% showed F0. No signs of necrosis were observed compared with OHa. Conclusions: Interaction among steatosis induced by MCD diet and OHa increases steatosis, at broader areas of the hepatic parenchyma with increased number of inflammatory foci, but no increase in ballooning, and a lower number of liver showed fibrosis compared to MCD.