Given the comprehensive examination of the role of fatty acid-rich diets in central nervous system development in children, this study bridges significant gaps in the understanding of dietary effects on neurodevelopment. It delves into the essential functions of fatty acids in neurodevelopment, including their contributions to neuronal membrane formation, neuroinflammatory modulation, neurogenesis, and synaptic plasticity. Despite the acknowledged importance of these nutrients, this review reveals a lack of comprehensive synthesis in current research, particularly regarding the broader spectrum of fatty acids and their optimal levels throughout childhood. By consolidating the existing knowledge and highlighting critical research gaps, such as the effects of fatty acid metabolism on neurodevelopmental disorders and the need for age-specific dietary guidelines, this study sets a foundation for future studies. This underscores the potential of nutritional strategies to significantly influence neurodevelopmental trajectories, advocating an enriched academic and clinical understanding that can inform dietary recommendations and interventions aimed at optimizing neurological health from infancy.

The objective of this work is to present a new procedure for the analysis of pesticides in water samples with use of solid phase extraction (SPE) and high performance chromatography with diode array detection (HPLC-DAD) and thin layer chromatography with diode array scanning (TLC-DAD). Pesticides were enriched from lakes water samples by solid phase extraction (SPE) on C18/SDB-1, C18, C18 Polar Plus, and CN cartridges. SPE was used not only for preconcentration of analytes but also for their fractionation. The analytes were eluted with methanol, and next with dichloromethane. Methanol eluates were analysed by HPLC-DAD, the dichloromethane eluates with TLC-DAD. The method was validated for precision, repeatability, and accuracy. The calibration plots were linear between 0.1 and 50.0 µg mL⁻¹ for all pesticides, the correlation coefficients, r, were between 0.9992 and 1.000, as determined by HPLC-DAD. In the TLC experiments, the best fit for the calibration lines was found when the calibration data were analyzed using a second degree polynomial regression. Calibration plots lay between 0.1 and 17 µg spot⁻¹ for all pesticides, the correlation coefficients, r, were between 0.9974 and 0.9997, as determined by TLC-DAD. The limit of detection (LOD) was between 0.04 and 0.65 µg spot⁻¹ (TLC-DAD) and between 0.02 and 1.56 µg mL⁻¹ (HPLC-DAD).

The aim of this review is to summarize the current knowledge on the use of coumarin-derived compounds in the zebrafish (Danio rerio) model. Coumarins, a class of naturally occurring compounds with diverse biological activities, including compounds such as coumarin, angelicin, and warfarin, have attracted considerable attention in the study of potential therapeutic agents for cancer, central nervous system disorders, and infectious diseases. The capabilities of coumarins as active compounds have led to synthesizing various derivatives with their own properties. While such variety is certainly promising, it is also cumbersome due to the large amount of research needed to find the most optimal compounds. The zebrafish model offers unique advantages for such studies, including high genetic and physiological homology to mammals, optical transparency of the embryos, and rapid developmental processes, facilitating the assessment of compound toxicity and underlying mechanisms of action. This review provides an in-depth analysis of the chemical properties of coumarins, their mechanisms of biological activity, and the results of previous studies evaluating the toxicity and efficacy of these compounds in zebrafish assays. The zebrafish model allows for a holistic assessment of the therapeutic potential of coumarin derivatives, offering valuable insights for advancing drug discovery and development.

High-fat diet (HFD)-induced obesity is a global health concern associated with gastrointestinal disorders. While mammalian models have elucidated the effects of a HFD on intestinal structure and function, its impact on zebrafish, a crucial model for studying diet-induced obesity and gastrointestinal dysfunction, remains inadequately characterized. This study investigated the influence of a HFD on zebrafish intestinal morphology, tight junction (TJ) protein expression, and inflammatory markers. Zebrafish fed a control diet or HFD with 40% or 60% fat exhibited significant alterations in intestinal morphology, with increased villi number but reduced villi width and length, suggesting compensatory responses to dietary stress. TJ protein expression (Claudin 2, Claudin 3, and Claudin 10) showed complex changes, particularly in the HFD60 juvenile group, indicating a multifaceted response in barrier integrity. Pro-inflammatory cytokine IL-6 and TNF-α levels were lower in both the juvenile and adult HFD60 groups than in the HFD40 and control groups, while elevated anti-inflammatory IL-10 levels in HFD60 adult zebrafish suggested activation of compensatory mechanisms. These findings highlight zebrafish as a valuable model for studying the effects of HFD on intestinal health and provide insights into the relationship between dietary fat, gut dysfunction, and inflammation.

Fatty acid-binding protein 4 (FABP4) has emerged as a multifunctional regulator in cancer biology, linking dysregulated lipid metabolism, immune modulation, and tumor progression. Initially recognized for its role in fatty acid transport and lipid homeostasis, FABP4 is now understood as a secreted adipokine that influences diverse oncogenic processes, particularly in adipose-rich tumor microenvironments. It is upregulated in various cancers and secreted by both tumor and cancer-associated fibroblasts. FABP4 facilitates lipid transfer, promotes fatty acid oxidation, and reprograms cancer cell metabolism. It also contributes to the crosstalk between tumor-associated macrophages, T-cells, and dendritic cells. FABP4 also supports epithelial-mesenchymal transition, enhances tumor cell plasticity, promotes invasion and metastasis, and has an impact on therapeutic resistance. The inhibition of FABP4 using small-molecule inhibitors or monoclonal antibodies has shown promise in restoring therapeutic sensitivity and reducing metastasis in preclinical models. FABP4 has emerged as a potential diagnostic and prognostic biomarker that predicts poor outcomes in multiple cancer types, supporting risk stratification and noninvasive diagnostics. Together, these findings place FABP4 at the intersection of tumor metabolism, immune evasion, and therapy resistance, highlighting its potential as both a biomarker and a therapeutic target in precision oncology and personalized medicine.

FABP4 (fatty acid-binding protein 4) is a lipid chaperone and secreted adipokine linking dysregulated fatty acid handling with inflammation, cellular stress, and insulin resistance in obesity. By modulating nuclear receptor signaling (notably PPARγ) and enhancing NF-κB/MAPK activation in adipocytes and macrophages, FABP4 contributes to maladaptive adipose remodeling and systemic metabolic decline. This review critically summarizes recent preclinical evidence on natural bioactive compounds that regulate FABP4 expression and associated adipogenic programs in models of adipogenesis and diet-induced obesity. Data from 3T3-L1/OP9 adipocytes, rodent studies, and selected alternative models indicate that many plant-derived extracts and phytochemicals (e.g., polyphenols, saponins, coumarins, terpenoids, and fermented products) down-regulate FABP4 at mRNA and/or protein levels. These effects are frequently accompanied by suppression of PPARγ/C/EBPα/SREBP1c signaling, activation of AMPK-related pathways, reduced lipid accumulation, and improved metabolic outcomes including lower weight gain, reduced adipocyte hypertrophy, improved steatosis, and favorable serum lipid profiles. Natural compounds from non-plant sources (animal- and microbe-derived metabolites) further broaden FABP4-targeting strategies, supporting FABP4 as a cross-class therapeutic node. Key translational barriers include poor extract standardization, incomplete identification of active constituents, limited oral bioavailability, microbiome-dependent variability, and scarce clinical validation. Future work should prioritize well-characterized lead scaffolds, targeted delivery, rational combinations, and standardized, adequately powered clinical trials assessing dose, durability of FABP4 suppression, and cardiometabolic safety.