Background and aim: Obesity and alcohol consumption are two of the main risk factors in liver diseases, which coexist frequently and are considered to accelerate the progression of liver damage, from simple steatosis to steatohepatitis, cirrhosis and cancer. The Mexican diet is high in cholesterol, in addition to being frequently found elevated in patients and animal models with obesity. Therefore, our goal is to determine the effect of alcohol intake in an environment with cholesterol overload.
Material and methods: Male and female mice of the C57BL / 6J strain 8-10 weeks old were used. The NIAAA model was used, which consists of consuming a Lieber-DeCarli diet added with ethanol (5% v / v final concentration) for 10 days, followed by acute dose intra-gastric (5g / kg) of ethanol. Cholesterol overload was induced by adding cholesterol (1.25 w / v) to the liquid diet. Liver damage was assessed using liver function tests. Biochemical tests were carried out to determine the degree of apoptosis and the amount of cholesterol in the different experimental groups.
Results: The alcoholic diet added with cholesterol exacerbates liver damage and causes premature death of males. Also, the enzymatic activity of ALT and AST were increased, both in males and in females groups. Liver caspase 3 activity, indicative of apoptosis, was also found increased with respect to the other groups. At the macroscopic level, a liver with higher steatosis was observed in the group treated with alcohol and cholesterol, data that was corroborated by H&E in histological sections with a 5.15-fold increase in the total cholesterol content in the liver compared to the control group. Females had higher liver cholesterol content than males (18.66μg cholesterol / mg protein vs. 15.6μg cholesterol / mg protein), however, the activity of transaminases were similar in both genders.
Conclusions: The data obtained suggests that liver cholesterol overload increases susceptibility to alcohol damage. An increase in cell death was observed in this group, as well as in liver damage tests. Further studies are required to determine the mechanism by which greater damage is caused in the presence of both agents.
Conflicts of interest: The authors have no conflicts of interest to declare.
