Cell death inducing DNA fragmentation factor-alpha-like A (Cidea) is a member of cell death-inducing DFF45-like effector (CIDE) protein. The initial function of CIDE is the promotion of cell death and DNA fragmentation in mammalian cells. Cidea was recently reported to play critical roles in the development of hepatic steatosis. The purpose of present study is to determine the effect of chronic alcohol intake on Cidea expression in the livers of mice with alcoholic fatty liver disease. Cidea expression was significantly increased in the liver of alcohol-induced fatty liver mice. While, knockdown of Cidea caused lipid droplets numbers reduction. Next, we detected the activity of ALDH2 reduction and the concentration of serum acetaldehyde accumulation in our alcohol-induced fatty liver mice. Cidea expression was elevated in AML12 cells exposed to 100uM acetaldehyde. Interestingly, Dual-luciferase reporter gene assay showed that 100 uM acetaldehyde led to the activation of Cidea reporter gene plasmid which containing SRE element. What’s more, the knockdown of SREBP1c suppressed acetaldehyde-induced Cidea expression. Overall, our findings suggest that Cidea is highly associated with alcoholic fatty liver disease and Cidea expression is specifically induced by acetaldehyde, and this up-regulation is most likely mediated by SREBP1c.

This study aimed to clarify whether low-dose ethanol intake could prevent high-fat diet-induced adverse effects on cardiomyocytes in mice.

Objectives: Our goal was to contribute to the production of reference values ​​of plasma or serum biochemical markers by determining the reference values ​​of gamma-glutamyltransferase (GGT), aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) in young Congolese presumed to be healthy. Methods: 250 young Congolese presumed to be healthy (125 boys and 125 girls) aged 15 to 25 participated in the study. They were selected according to anamnestic and clinico-biological criteria. Samples were taken on a tube containing EDTA and the resulting plasma was stored at -20 ° C. The KENZA MAX spectrophotometer was used to analyze GGT, ASAT and ALAT. The median and the 2.5-97.5 percentiles were used to set the reference limits for each enzyme. The benchmarks determined were compared with those reported by other Africans, Europeans, Indians and Americans. Results: The established reference values ​​were: GGT 12.15-61.85 IU/L for boys and 7-51.95 IU / l for girls (p˂0.0001); ASAT 21.60-94.85 IU/L for boys and 17-84.85 IU/L for girls (p = 0.0003); ALAT 8.30-74.40 IU/L for boys and 8-53.85 IU/L for girls (p˂0.0001). In addition, the comparison between our values ​​and those of other populations showed significant differences. Conclusion: Our results underline the importance of establishing reference values ​​for plasma enzymes specific to the Congolese population. The use of the values ​​established in the ’other populations could induce errors of judgment by excess or by default. Key words: Gamma-glutamyltransferase, Aspartate aminotransferase, Alanine aminotransferase, Reference values, Congo.