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

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.