Amino acids tyrosine (Tyr) and tryptophan (Trp) play a significant role in the regulation of energy metabolism, locomotor activity, and eating behavior. We studied the possibility of modulating these processes in obesity by increasing the pool of Tyr and Trp in the experimental diet. As a model of obesity, we used Wistar rats fed a diet with an excess specific energy value (HFCD) for 64 days. Trp led to a normalization of the rats’ body weight almost to the control level, but increased anxiety-like behavior and decreased long-term memory. The consumption of amino acids resulted in increased grip strength and impairment of short-term memory. The locomotor activity of animals decreased with age as a result of Tyr consumption, while Trp, on the contrary, prevented this. The Tyr supplementation led to the normalization of triglycerides and LDL. In the spleen cell lysates, amino acids suppressed the production of proinflammatory cytokines. The liver tissue morphology showed that the consumption of Tyr noticeably weakened the signs of fatty degeneration. The addition of Trp, on the contrary, led to an unfavorable effect, consisting of the appearance of a high number of large rounded fatty vacuoles. The data obtained indicate a more pronounced anti-inflammatory effect of Tyr as compared to Trp.

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.

Non-alcoholic fatty liver disease (NAFLD) is among the most prevalent liver disorders globally, affecting approximately 25% to 40% of the adult population. Closely associated with metabolic syndrome, obesity, insulin resistance, and dyslipidemia, NAFLD presents a growing burden due to its increasing incidence and high healthcare costs. In this context, the development of effective preventive and therapeutic strategies remains a pressing challenge in modern medicine. This review aims to analyze current scientific evidence on bioactive plant compounds—particularly polyphenols and polyprenols—including their natural sources, mechanisms of action, and potential applications in the prevention and dietary management of NAFLD. A growing body of evidence demonstrates that both polyphenols and polyprenols exert hepatoprotective, antioxidant, anti-inflammatory, and hypolipidemic effects. These compounds modulate signaling pathways implicated in hepatic steatosis and fibrosis, positively influence gut microbiota composition, and affect bile acid metabolism. Studies have confirmed the efficacy of polyphenol-rich foods (naringenin, resveratrol, chlorogenic acid, etc.) and polyprenol-based formulations in reducing body weight and liver steatosis, improving biochemical markers and insulin resistance. The combined application of polyphenols and polyprenols may yield synergistic effects on multiple pathogenic pathways and represents a promising direction for the dietary prevention and management of NAFLD.

Oxidative stress can be caused by bad nutrition, psychoemotional stress, or other external influences in everyday life. The aim of this study is to develop and verify biological models using male Wistar rats that allow reproducing oxidative stress in vivo, in particular: food (diet with high cholesterol and fructose content), medical (injection of CCl₄), and physiological (immobilization stress). Diet with 1% cholesterol and fructose had the greatest impact on the antioxidant status of animals: a significant increase in serum malondialdehyde (by 1.8 times) and superoxide dismutase (by 2.4 times) as well as a significant decrease in the Cat gene expression by 35% were shown. The immobilization led only to a significant decrease in serum lipid peroxides by 29%. A single intraperitoneal administration of CCl₄ was accompanied by a significant increase in the blood lipid peroxides (by 1.3 times) and catalase (by 1.6 times), as well as a significant decrease in the Cat mRNA by 33% and Gpx1 by 48%. The obtained data can be used to study the effectiveness of drugs, biologically active food supplements and functional nutrition in vivo.

Dihydroquercetin (3,5,7,3',4'-pentahydroxy-flavanone) is known for its powerful antioxidant, organ-protective, and antiinflammatory activities that can be applied to heavy-metal intoxication. The present research objective was to evaluate the possible protective potential of dietary dihydroquercetin in a rat model of subacute (92 days) intoxication with nickel nanoparticles. The experiment involved five groups of twelve male Wistar rats in each. Group 1 served as control. Other groups received nickel nanoparticles as part of their diet. Groups 2 and 4 received nickel nanoparticles with an average diameter of 53.7 nm (NiNP1), while groups 3 and 5 were fed with nanoparticles with an average diameter of 70.9 nm (NiNP2). The dose was calculated as 10 mg/kg b.w. Groups 4 and 5 also received 23 mg/kg b.w. of water-soluble stabilized dihydroquercetin with drinking water. After the dihydroquercetin treatment, the group that consumed 53.7 nm nickel nanoparticles demonstrated lower blood serum glucose, triglycerides, low-density lipoprotein cholesterol, and creatinine. Dihydroquercetin prevented the increase in total protein and albumin fraction associated with nickel nanoparticles intake. The experimental rats also demonstrated lower levels of pro-inflammatory cytokines IL-1β, IL-4, IL-6, and IL-17A, as well as a lower relative spleen weight after the treatment. In the group exposed to 53.7 nm nickel nanoparticles, the dihydroquercetin treatment increased the ratio of cytokines IL-10/IL-17A and decreased the level of circulating FABP2 protein, which is a biomarker of increased intestinal barrier permeability. In the group that received 70.9 nm nickel nanoparticles, the dihydroquercetin treatment inhibited the expression of the fibrogenic Timp3 gene in the liver. In the group that received 53.7 nm nickel nanoparticles, dihydroquercetin partially improved the violated morphology indexes in liver and kidney tissue. However, dihydroquercetin restored neither the content of reduced glutathione in the liver nor the indicators of selenium safety, which were suppressed under the effect of nickel nanoparticles. Moreover, the treatment failed to restore the low locomotor activity in the elevated plus maze test. Dihydroquercetin treatment showed some signs of detoxication and anti-inflammation in rats subjected to nickel nanoparticles. However, additional preclinical studies are necessary to substantiate its prophylactic potential in cases of exposure to nanoparticles of nickel and other heavy metals.

C57black/6J female mice were fed an isocaloric diet with excess fat, fructose, cholesterol, or combinations of them for 62 days. In their liver, the differential expression of 30 003 genes...