Abstracts of the 2023 Annual Meeting of the ALEH
More infoMetabolic disorders and alcohol consumption are the most common etiological agents in hepatic steatosis (HS). Metabolic alterations, oxidative stress, and inflammation are key mechanisms in the development of this disease. There is a few evidence that demonstrates the synergistic effects generated by both etiological agents. N-acetyl cysteine (NAC) is an antioxidant used clinically, whose efficacy in HS development induced by a hypercaloric diet plus alcohol consumption is unknown. This study aimed to evaluate NAC effects on oxidative stress, and metabolic alterations induced in HS generated by ethanol chronic consumption plus a hypercaloric diet in a mouse model.
Materials and MethodsMale mice (C57BL/6J, n=4) were divided into 3 groups. 1) Control, mice fed with a conventional diet and water ad libitum; 2) HF/OH, mice fed a hypercaloric diet, and 20% ethanol; 3) HF/OH+NAC, mice with the same treatments of HF/OH group, and NAC (300 mg/kg/day, p.o.). All treatments lasted 5 months. Serum biochemical markers were determined: AST, ALT, cholesterol, HDL, LDL, triglycerides, leptin, ghrelin, insulin, resistin, and GLP1; also, oxidative stress parameters such as MDA, and SOD, CAT and Nrf2 proteins expression were analyzed through colorimetric assays, and western blot. Finally, H&E staining was performed in liver samples.
ResultsNAC prevents weight gain and metabolic alterations generated by concomitant consumption of a hypercaloric diet and alcohol; it also modulates changes in anorexigenic and orexigenic adipokines. On the other hand, NAC reduces the oxidative environment induced by both etiological agents and prevents tissue alterations in hepatic parenchyma.
ConclusionsNAC ameliorates alterations in processes related to establishment of HS induced by ethanol chronic consumption plus a hypercaloric diet. Its pharmacodynamic mechanisms go beyond its antioxidant capacity.
