Volume: 5, 2026
5th International PhD Students’ Conference at the University of Life Sciences in Lublin, Poland:
ENVIRONMENT – PLANT – ANIMAL – PRODUCT
Abstract number: A032
DOI: https://doi.org/10.24326/ICDSUPL5.A032
Published online: 22 April 2026
Biochemical pathways and innovative therapeutic strategies in alimentary toxicosis and metabolic disorders
Vladyslav Rodz*, Bohdan Butenko, Anna Pashynska and Liliia Kalachniuk
Department of Biochemistry, National University of Life and Environmental Sciences of Ukraine, 15 Heroiv Oborony St., 03041, Kyiv, Ukraine
* Corresponding author: vlad.rodz150@gmail.com
The vulnerability of the body to metabolic disorders under conditions of obesity is closely linked to the activity of the intestinal microbiota, which serves as the primary source of systemic D-lactate. Unlike the L-isomer, microbial D-lactate more intensively stimulates hepatic gluconeogenesis and lipogenesis, leading to persistent hyperglycemia and the development of fatty liver disease. One of the most promising therapeutic mechanisms is the “substrate trap” within the intestinal lumen, created using a biocompatible polymer (poly-L-lactide). This trap specifically binds D-lactate, preventing its entry into the systemic circulation and forcing the body to excrete it via feces. Such sequestration of the substrate effectively lowers glucose levels, reduces insulin resistance (HOMA-IR index), and mitigates liver inflammation and fibrosis.
Chocolate toxicity in exotic species (small mammals, birds, and reptiles) poses a significant threat due to pronounced species-specific reactions and limited diagnostic tools. The pathological impact of methylxanthines provokes systemic disturbances of homeostasis, which, given the lack of data on the metabolism of these animals, requires immediate supportive therapy. A key objective remains the systematization of species-specific indicators to optimize the clinical management of these vulnerable patients.
Food poisoning caused by cereal mycotoxins, particularly deoxynivalenol (DON), triggers intense oxidative stress accompanied by a massive surge of reactive oxygen species (ROS) and the depletion of natural cellular defenses. In response to such toxic stress, the Nrf2/ARE pathway becomes a key regulatory mechanism, initiating the expression of antioxidant defense genes to restore cellular homeostasis. Research on the Lactobacillus rhamnosus MY-1 strain demonstrates the possibility of effectively managing this process: the probiotic supernatant reduces MDA levels and restores superoxide dismutase (SOD) activity and total antioxidant capacity (T-AOC). This approach to regulating cellular activity in vitro represents a promising strategy for protection against alimentary toxicity in veterinary medicine.
Conclusion. Effective correction of metabolic and toxic states today is based on the implementation of intestinal traps for D-lactate, species-specific management of toxicosis in exotic animals, and the activation of the Nrf2/ARE antioxidant pathway using probiotic metabolites for cellular protection.
Keywords: alimentary toxicosis; D-lactate; metabolic disorders; mycotoxins; Nrf2/ARE pathway
How to cite
Rodz V., Butenko B., Pashynska A., Kalachniuk L., 2026. Biochemical pathways and innovative therapeutic strategies in alimentary toxicosis and metabolic disorders. In: 5th International PhD Students’ Conference at the University of Life Sciences in Lublin, Poland: Environment – Plant – Animal – Product. https://doi.org/10.24326/ICDSUPL5.A032
