Non-alcoholic fatty liver disease (NAFLD) is currently estimated as the most prevalent chronic liver disease in all age groups. An increasing body of evidence obtained in experimental and clinical data indicates that oxidative stress is the most important pathogenic factor in the development of NAFLD. The study aimed to investigate the impact of α-lipoic acid (LA), widely used as an antioxidant, on the effects of a hypercaloric choline-deficient diet. Male Wistar rats were divided into three groups: control diet (C); hypercaloric choline-deficient diet (HCCD), and hypercaloric choline-deficient diet with α-lipoic acid (HCCD+LA). Supplementation of HCCD with LA for eight weeks led to a decrease in visceral adipose tissue/body weight ratio, the activity of liver glutathione peroxidase and paraoxonase-1, plasma, and liver total antioxidant activity, as well as an increase in liver/body weight ratio, liver total lipid and triglyceride content, and liver transaminase activities compared to the HCCD group without LA. In conclusion, our study shows that α-lipoic acid detains obesity development but exacerbates the severity of diet-induced oxidative stress and lipid accumulation in the liver of male Wistar rats fed a hypercaloric choline-deficient diet.

The beneficial effect of polyphenol resveratrol (RES) on liver diseases, including non-alcoholic fatty liver disease (NAFLD), has been reported in numerous studies. De novo lipogenesis in the liver is considered as one of the possible molecular mechanisms for the development of obesity and NAFLD. This work aimed to study the effect of RES on the development of NAFLD and to evaluate the expression of carbohydrate and lipid metabolic key enzymes genes in rats fed on a high-fat high-fructose diet (HFHFrD). For 10 weeks, the control group of Wistar male rats received a standard diet and water; three experimental groups were fed on HFHFrD. The rats in the 2nd and 3rd experimental groups received RES at a daily dose of 10 and 100 mg/kg body weight, respectively. A histological examination of the liver was carried out and the expression of carbohydrate (Khk, Gck, Pklr) and lipid (Acaca, Fasn, Scd) metabolizing enzymes and transcription factors (Mlxipl, Srebf1, Ppara) genes was studied. The consumption of HFHFrD led to the development of NAFLD, accompanied by an increase in Gck gene expression, a decrease in Pklr, Acaca, Fasn, Scd. RES in both doses had no effect on the development of NAFLD, as well as on the expression of the studied genes.

The toxic effects of nickel nanoparticles (NiNPs) in their 92-day oral administration to male Wistar rats at doses of 0.1, 1 and 10 mg/kg body weight were evaluated. An increase in glycemia, triglyceride, LDL, total protein, and its globulin fraction levels were noticed in NiNPs exposed rats. NiNPs caused a decrease in reserves of liver glutathione and excretion of selenium in the urine, and an increase in serum levels of cytokines IL-1β, IL-2, IL-6, IL-12p70, TNF-α, and INF-γ, with a simultaneous decrease in IL-17A as well as increased fibrosis-marking gene and Tp53 expression.