Halina Tkaczenko

Glucagon-like peptide-1 (GLP-1) has emerged as a key regulator of metabolic, inflammatory and oxidative homeostasis, extending beyond its traditional function as an incretin hormone. This narrative review summarises the latest evidence from two decades of research into the role of GLP-1 in redox biology and metabolic regulation in tissues affected by obesity, type 2 diabetes and metabolic dysfunction-associated steatotic liver disease. There is growing evidence that GLP-1 signalling modulates multiple oxidative pathways, including AMPK-dependent metabolic reprogramming, mitochondrial quality control, nitric oxide–cGMP signalling, the regulation of ferroptosis, and the suppression of inflammatory pathways such as the NLRP3 inflammasome. Through these mechanisms, GLP-1 contributes to maintaining cellular redox balance, mitochondrial resilience, and metabolic adaptation in conditions of chronic oxidative stress. The review also emphasises the complementary function of GLP-1 receptor agonists (GLP-1RAs) and natural bioactive compounds such as polyphenols, anthocyanins, terpenoids and omega-3 fatty acids. These compounds may reinforce antioxidant defences, reduce inflammatory signalling and support mitochondrial function. Particular attention is given to the role of the gut microbiota in determining GLP-1 responsiveness. Gut microbiota-derived metabolites, including short-chain fatty acids (SCFAs) and bile acid derivatives, contribute to incretin secretion, intestinal barrier maintenance, and systemic redox regulation. This review integrates endocrinology, oxidative stress biology, microbiome science and nutritional biochemistry to provide a comprehensive framework describing GLP-1 as a multi-organ metabolic signal that coordinates endocrine, immune, mitochondrial and redox pathways. These insights will inform the development of future therapeutic strategies that combine GLP-1-based pharmacology with precision nutrition and microbiome-targeted approaches, with the aim of improving metabolic resilience and addressing the oxidative dysregulation associated with chronic metabolic diseases.

Beetroot (Beta vulgaris L.) is a rich source of dietary nitrates, polyphenols, and other bioactive compounds that have potential cardiovascular, metabolic, and health-promoting effects. While previous reviews have largely focused on the nitrate-derived nitric oxide (NO) signalling pathway or the antioxidant properties of the pigments known as ‘betalains’, there is an increasing body of evidence that suggests microbial transformation and fermentation can substantially modify the biological properties of beetroot. This narrative review summarises the latest research on beetroot phytochemistry, nitrate–nitrite–NO metabolism, microbial biotransformation, fermentation and host physiological responses. Particular attention is given to the impact of fermentation on phenolic compounds, betalains, and the metabolism of nitrates and nitrites, as well as to its effects on antioxidant activity, bioaccessibility, and interactions with the gut microbiome. The available evidence suggests that fermentation can alter the beetroot matrix, increasing the accessibility or recovery of certain bioactive compounds while producing additional microbial metabolites with potential biological activity. These changes may complement the well-established effects of beetroot-derived nitrates and betalains on vascular function, redox homeostasis, inflammation and exercise-related physiology. However, evidence specifically linking fermented beetroot to clinical outcomes is limited, and the effects of fermentation depend heavily on microbial strains, processing conditions, the food matrix and host characteristics. Interindividual differences in microbiome composition may further contribute to variability in responses to beetroot-derived compounds. Thus, fermentation is a promising strategy for increasing the functional potential of beetroot by altering the bioaccessibility of its bioactive constituents through microbial biotransformation. Further well-designed human studies are needed to establish whether these compositional and mechanistic changes result in clinically significant benefits, and to clarify how individual microbiome profiles contribute to responses to fermented beetroot.

Background/Objectives: Glucagon-like peptide-1 (GLP-1), which is released by enteroendocrine L-cells, is the primary incretin hormone and plays a pivotal role in glucose regulation, appetite control, and metabolic health. While GLP-1 receptor agonists offer significant therapeutic benefits, there is a growing interest in identifying foods that can increase endogenous GLP-1 production through physiological processes. However, the physiological impact of modulating GLP-1 through diet is modest compared with activating GLP-1 receptors pharmacologically. This narrative review summarizes the latest reports on how specific food matrices and gut microbiota-dependent pathways influence GLP-1 release, emphasizing their importance in precision nutrition. Methods: Literature published between 2001 and 2026 was reviewed, including experimental, clinical, and translational studies examining the effects of foods on GLP-1 secretion, L-cell activation, nutrient-sensing receptors, microbial metabolites, and metabolic outcomes. Evidence was synthesized for food categories such as fermented dairy products, fermented vegetables, whole grains, legumes, fiber-rich root vegetables, berries, grapes, green tea, turmeric and oily fish. Results: Foods modulate endogenous GLP-1 secretion through complementary pathways involving L-cell stimulation and the activation of receptors, including FFAR2, FFAR3, GPR119, TGR5 and FFAR4 (GPR120), as well as the production of microbial metabolites. Fermented dairy products, kimchi, kefir, Jerusalem artichokes, chicory root, oats, garlic, onions, berries, grapes, green tea and oily fish support incretin regulation through microbial fermentation, the generation of short-chain fatty acids (SCFAs), bile acid signalling and the release of bioactive compounds. These food matrices shape metabolite profiles more effectively than isolated nutrients, highlighting the importance of the interaction between whole foods and the gut microbiota. Conclusions: Foods rich in fermentable substrates, polyphenols, bioactive peptides and omega-3 fatty acids are promising dietary modulators of physiological GLP-1 activity. Taking into account microbiome characteristics, metabolic phenotype and individual postprandial responses could facilitate the development of personalized nutrition strategies to help prevent and manage obesity, type 2 diabetes and related cardiometabolic disorders.

Purpose of the work. This article aims to analyse the health-promoting benefits of Ceylon cinnamon (Cinnamomum verum J. Presl) and evaluate its therapeutic value in contemporary medical and dietary contexts. It also discusses potential applications in preventing and supporting the treatment of metabolic, cardiovascular, neoplastic, neurodegenerative and infectious diseases, as well as digestive and skeletal system disorders. Additionally, the study assesses the safety of using cinnamon in various pharmaceutical and dietary forms. Methodology. A review of the available scientific literature was conducted to obtain comprehensive information on the medicinal properties and potential applications of Ceylon cinnamon. The analysis included the following databases: PubMed Central, Scopus, ResearchGate, Web of Science, ScienceDirect, Ovid Technologies and Google Scholar. A total of 139 scientific articles and eight monographs were included in the review. The analysed materials comprised original research articles, systematic reviews, meta-analyses and experimental and clinical reports, which addressed the effects of the chemical compounds present in cinnamon on its therapeutic properties. Source selection was based on publication recency, methodological quality, and the clinical relevance of the reported findings. Scientific novelty. This work offers a novel perspective on the health benefits of C. verum, highlighting its potential as an adjunctive therapy for cancer, metabolic, infectious and neurodegenerative diseases. The article presents research findings that indicate the broad spectrum of activity of the bioactive compounds found in cinnamon, and their potential application in clinical practice. Particular attention is given to the molecular mechanisms of phytochemical action and the use of modern technologies to enhance bioavailability and therapeutic efficacy, such as nanoparticles and mucoadhesive gels. Combining botanical, pharmacological, and clinical knowledge using an interdisciplinary approach enabled a holistic assessment of the therapeutic potential of Ceylon cinnamon. Conclusions. Cinnamon has been used in Asian cuisine for several thousand years, not only as a spice, but also as a medicinal ingredient. It is characterised by its rich phytochemistry and wide range of health-promoting effects. C. verum alleviates disorders of the digestive, urinary and skeletal systems, and exhibits strong antioxidant and anti-inflammatory properties. Available data suggest that it may support the treatment of numerous diseases, including cancer, due to its antioxidant content and ability to modulate inflammatory processes. Its documented biological activities – anti-inflammatory, antiviral, antibacterial, antiparasitic, anti-obesity and antineurodegenerative – have a beneficial impact on human health. Compounds present in cinnamon essential oils improve tissue insulin sensitivity, reduce blood glucose and lipid levels, and inhibit the development of neoplastic and infectious processes. The use of modern delivery systems for bioactive substances, such as nanoparticles and mucoadhesive gels, can significantly increase the bioavailability and therapeutic efficacy of cinnamon while reducing its toxicity to normal cells. Furthermore, taking cinnamon supplements at doses of 1-6 g per day has been shown to have the most favourable health effects. Products derived from the bark, leaves and roots of the cinnamon tree are used in herbal medicine, cosmetology and the food and beverage industry.

Mycotoxins are toxic secondary metabolites produced by filamentous fungi that often contaminate plant-based feed ingredients used in aquaculture. The ongoing replacement of fishmeal and fish oil with cereals and oilseeds increases the risk of fish being chronically exposed to multiple mycotoxins. This review aims to provide a short overview of mycotoxin contamination in aquaculture systems. This review summarises the occurrence, exposure routes, toxicokinetics, and biological effects of the main regulated mycotoxins, such as aflatoxin B1 (AFB1), deoxynivalenol (DON), zearalenone (ZEN), fumonisins, and ochratoxin A (OTA), as well as emerging compounds, including beauvericin (BEA), enniatins (ENNs), and Alternaria toxins. Although environmental factors and post-harvest processes may also contribute, feed is identified as the primary contamination source. Mycotoxins show limited carry-over into fish tissues, with the liver being the main site of accumulation and biotransformation; meanwhile, muscle residues remain relatively low, yet still relevant in terms of food safety. The toxic effects are multifactorial and include oxidative stress, apoptosis, immune dysregulation, endocrine disruption and metabolic disorders. There is increasing evidence highlighting the importance of co-exposure scenarios, where additive or synergistic interactions can enhance toxicity. The study of emerging and modified ('masked') mycotoxins remains insufficient, especially in vivo, which complicates risk assessment. Conclusions: Improved monitoring, a better understanding of combined toxicity, and the harmonisation of regulatory limits are essential. The development of effective mitigation strategies is necessary to ensure the sustainability of aquaculture production and food safety, particularly in the context of an increasing reliance on plant-based feeds. Keywords: mycotoxins; aquaculture; fish health; oxidative stress; carry-over; food safety; mixture toxicity; risk assessment.

Ischemic stroke triggers a severe redox disequilibrium that critically shapes cell survival within the penumbra. Although oxidative DNA damage arises from excessive ROS production, the capacity to repair such lesions is tightly constrained by cellular metabolic status. Growing evidence indicates that astrocytes, key metabolic regulators of the neurovascular unit, modulate neuronal susceptibility to genomic injury through redox buffering, NAD⁺ maintenance, and metabolic support. In the metabolically impaired yet structurally preserved penumbra, astrocytic control of glutathione turnover, mitochondrial function, and lactate shuttling may determine whether oxidative DNA lesions are efficiently repaired or progress toward energetic collapse. Poly(ADP-ribose) polymerase 1 activation following DNA strand breaks couples genomic stress to NAD⁺ depletion and bioenergetic failure, forming a critical interface between redox biology and metabolism. This framework posits that astrocytes preserve genomic integrity not by directly altering DNA repair pathways but by sustaining the energetic capacity required for an effective DNA damage response. Elucidating this astrocyte-centered redox–metabolic axis may reveal therapeutic strategies to stabilize penumbral tissue and improve stroke outcomes.

Microplastics and nanoplastics (MNPLs) are increasingly recognized as dynamic vectors capable of transporting a wide range of environmental contaminants, as well as acting as physical particulates. Their small size, high surface reactivity and strong sorption capacity allow them to carry metals, pesticides, pharmaceuticals and endocrine-active compounds into biological systems. This narrative review examines how these particle-contaminant complexes influence oxidative stress, inflammatory signaling and endocrine function during early development. Relevant literature was identified through structured searches of PubMed, Scopus, Web of Science and Google Scholar, with a focus on the physicochemical properties of plastics, sorption mechanisms, gut barrier physiology and developmental toxicology. Early developmental stages are particularly sensitive, as immature mucus layers, permeable epithelial junctions and underdeveloped detoxification pathways facilitate the uptake and systemic distribution of MNPLs. Once internalized, these particles and their chemical cargo promote the generation of reactive oxygen species through redox-active contaminants, surface-catalysed reactions and mitochondrial dysfunction. The resulting oxidative imbalance activates stress-responsive pathways, including Nrf2–Keap1 signaling, and promotes lipid peroxidation, DNA damage and cellular dysfunction. MNPLs also stimulate inflammatory cascades by activating pattern-recognition receptors, altering cytokine profiles and disrupting epithelial homeostasis. These responses are intensified in the presence of sorbed pollutants, leading to sustained inflammatory states that can be particularly detrimental during organogenesis and immune maturation. Endocrine function is likewise affected, as MNPLs transport hormonally active chemicals and can interfere with hormone-responsive pathways through oxidative and inflammatory mechanisms. These interactions may disrupt thyroid signaling, metabolic regulation and the development of the reproductive axis, with potential long-term physiological consequences. Integrating evidence from polymer chemistry, contaminant behavior and developmental physiology, this review shows that MNPLs act as biologically active vectors that may increase oxidative, inflammatory and endocrine disturbances during early development. These findings highlight the importance of considering particle–contaminant interactions as a critical component of early-life risk assessment.

Adolescence is a developmental stage marked by dynamic interactions between diet, the gut microbiome and endocrine maturation, creating a physiological environment in which early metabolic disturbances can rapidly translate into long-term cardiovascular vulnerability. This narrative review summarises the latest research on the diet–microbiome–hormone axis in adolescents, focusing on the metabolic pathways through which microbial metabolites influence host physiology. Short-chain fatty acids (SCFAs), microbially transformed bile acids and postbiotic signalling molecules regulate enteroendocrine communication, insulin sensitivity, vascular function and inflammatory tone, thereby linking dietary exposures to early cardiometabolic alterations. Dysbiosis, driven by ultra-processed dietary patterns, low fibre intake and reduced microbial diversity, promotes metabolic endotoxemia, neuroendocrine imbalance and endothelial impairment, all of which are recognised as early indicators of cardiovascular disease. A distinctive contribution of this review is the integration of PF into the adolescent cardiometabolic framework. This emerging biotechnological process enables the controlled production of structurally defined bioactive compounds, including angiotensin-converting enzyme (ACE) inhibitory peptides, targeted prebiotic oligosaccharides, fermentable substrates that promote SCFA formation, microbially derived eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), phytosterols and purified postbiotics. These compounds modulate several regulatory pathways, such as the renin–angiotensin–aldosterone system, lipid and bile acid metabolism, gut barrier stability, inflammatory signalling and endocrine axes involving glucagon-like peptide-1 (GLP-1), peptide YY (PYY), leptin, insulin sensitivity and growth hormone/insulin-like growth factor-1 (GH/IGF-1) dynamics. By situating precision fermentation within the broader context of adolescent metabolic susceptibility, this review highlights its potential to support microbiome resilience, stabilise hormonal regulation and mitigate early cardiovascular risk. However, further adolescent-specific clinical trials and long-term safety assessments are required to translate these advances into effective public health strategies.

T-2 toxin, a type A trichothecene produced by Fusarium species, is one of the most toxic and environmentally persistent mycotoxins found in aquaculture feed. Despite growing evidence of its immunotoxic and oxidative effects in fish, its impact on tissue-specific lipid and protein metabolism, and the interrelationships between these biochemical pathways, remains poorly understood. This study examined the impact of dietary exposure to T-2 toxin (0.25 mg/kg feed; 5 MPC) on total lipid, phospholipid and protein concentrations in the gills, liver and brain of common carp (Cyprinus carpio). Correlation and regression analyses were also performed to identify coordinated metabolic responses and potential toxicity biomarkers. Exposure to T-2 toxin for 14 days induced pronounced, tissue-specific alterations in biochemical composition. The gills exhibited the most severe metabolic disruption, characterised by significant decreases in total lipids (p = 0.010; Cohen’s d = 2.24) and total proteins (p < 0.001; Cohen’s d = 3.32), indicating severe impairment of energy metabolism and protein homeostasis. In contrast, the brain showed a significant increase in total lipid content (p = 0.008; Cohen’s d = 2.22), suggesting altered lipid distribution and potential neurotoxic effects. Meanwhile, the liver displayed moderate changes, with a significant reduction in protein concentration (p = 0.031), but relatively stable lipid profiles. Despite metabolic disturbances, phospholipid levels remained largely unchanged across tissues, indicating the preservation of structural membrane components. Correlation and regression analyses revealed strong lipid–protein coupling in the gills (r = 0.83; R² = 0.69), moderate associations in the brain, and weak or absent relationships in the liver. This highlights differences in the regulation of metabolic networks across tissues. The gills emerged as the most sensitive organ, reflecting tightly coordinated metabolic responses to T-2 exposure. The results demonstrate that the T-2 mycotoxin disrupts systemic energy metabolism and protein homeostasis in C. carpio in a tissue-specific manner. The most pronounced effects were observed in the branchial tissue, alongside distinct lipid accumulation in the neural tissue. These findings identify total lipids and proteins in the gills and brain as sensitive biomarkers of T-2-induced metabolic disturbance, and emphasise the importance of an integrative, multi-tissue approach in the study of mycotoxin toxicity. The study also emphasises that the disruption of coordinated metabolic networks is a key component of T-2 toxicity in fish.