Search Results (288)

Background: Synaptic plasticity in neurodegenerative disorders (NDs), cognitive impairment, and mental health conditions is regulated by brain-derived neurotrophic factor (BDNF). Even healthy individuals have different levels, which are affected by complex epigenetic, inflammatory, and metabolic regulation. BDNF expression changes are associated with both typical and abnormal aging, as well as mental health conditions. These changes affect brain areas that are crucial for memory, such as the hippocampus and the parahippocampal cortex. Neurotrophins (NTs), including nerve growth factor (NGF) and BDNF, are essential for neuronal differentiation via tropomyosin receptor kinase B (TrkB) and the p75 neurotrophin receptor (p75NTR). Dysregulated NTs signaling contributes to synaptic dysfunction and neuroinflammation. Objective: This systematic review synthesizes preclinical evidence of the potential of naturally derived compounds to modulate NTs for neuroprotection and their incorporation into novel foods. Methodology: A review of major databases found studies that examined the impact of dietary polyphenols and other bioactive substances on NT signaling oxidative stress, inflammation, and neuronal plasticity. Results: Compounds such as epigallocatechin gallate, resveratrol, curcumin, quercetin, and flavanols, can positively impact NTs, reducing reactive oxygen species/reactive nitrogen species, enhancing cell survival, and increasing the expression of trophic factors such as nuclear factor erythroid 2-related factor 2 (Nrf2), NGF, and vascular endothelial growth factor in neural stem cells. However, their bioavailability, optimal dosage, and dietary interactions require further research. Conclusions: The consumption of BDNF-promoting foods can potentially stimulate BDNF synthesis, support optimal neurotransmission, and fortify neural plasticity. Evidence supports a polyphenol-rich diet for preventing NDs and promoting brain health. Observational studies consistently support the protective effects of polyphenols on brain health through their impact on the gut–brain axis. Full article

The sustainability, crop production, and food safety of agriculture are increasingly challenged by microplastic pollution, as agricultural soils are the largest reservoirs and may serve as points of contact for plastic particles in the food chain. This review provides a comprehensive overview of plant materials, fate and uptake pathways, detection techniques, and the possible risks of microplastics in agriculture. Agroecosystems are also a source of microplastics, such as plastic mulch films, sewage sludge, compost and manure additives, wastewater irrigation, polymer-coated fertilizers, greenhouse materials, atmospheric deposition, and decomposition of discarded agricultural plastics. Their distribution and mobility in soil are controlled by polymer composition, particle size, morphology, density, surface ageing, soil texture, organic matter content, tillage practices, runoff, leaching, and soil biota. Recent data show that microplastics, especially smaller microplastics and nanoplastics, can attach to root surfaces, penetrate plants via cracks in roots, areas of lateral root development, and apoplastic pathways, and eventually move to tissues aboveground. Plant tissue detection is often accomplished by digestion of the sample, density separation, visual and fluorescence microscopy, Fourier-transform infrared spectroscopy, Raman spectroscopy, pyrolysis–gas chromatography mass spectrometry, and electron microscopy, but standardization of these methods remains a significant challenge. Microplastics can disrupt seed germination, root structure, nutrient absorption, photosynthesis, oxidative homeostasis, biomass buildup, yield development, and quality. Further, their capacity to transport additives, plasticizers, heavy metals, and persistent organic pollutants raises concerns about the transfer of contaminants to edible plant parts and their potential transfer to human diets. Further studies are needed focusing on field-realistic exposure conditions, long-term crop–soil interactions, nanoplastics behaviour, standardised analysis procedures, uptake and translocation pathways, edible crop risk assessments, and sustainable mitigation approaches to reduce microplastics in agroecosystems. Full article

Growing evidence indicates that the gut microbiota is not a static ecosystem but a rhythmic metabolic organ whose oscillatory activity is tightly coordinated with host circadian biology. Disruption of this temporal alignment, through irregular diet, sleep disturbance, shift work, or social jet lag, may profoundly alter microbial composition and the production of neuroactive metabolites. These alterations have emerged as potential contributors to the pathophysiology of mood disorders. This review introduces the concept of chrono-metabolic psychiatry, a framework integrating circadian rhythms, gut microbiota dynamics, and host metabolic signaling in the development and course of depressive and bipolar disorders. In this framework, the term “chrono-metabolic” refers to the integration of biological timing, host metabolic regulation, and microbiota-derived metabolic signaling. Chrono-metabolic psychiatry therefore shifts the focus from static dysbiosis or neurotransmitter imbalance alone to the time-dependent interactions among circadian misalignment, microbial rhythmicity, immune regulation, metabolite production, and affective instability. Diurnal fluctuations in short-chain fatty acids, tryptophan–kynurenine metabolites, bile acids, and microbial-derived neurotransmitters interact with clock gene regulation, hypothalamic–pituitary–adrenal axis activity, neuroinflammation, and synaptic plasticity. Chrono-disruption may represent a transdiagnostic vulnerability factor and may confirm the bidirectional relationship between mood instability and microbiota rhythmicity. Emerging therapeutic implications, including chrono-nutrition, time-restricted feeding, targeted probiotic administration (“chronobiotics”), and the microbiota-modulating effects of psychotropic medications are discussed. By shifting from a compositional to a temporal–metabolic perspective, this model highlights the importance of microbial oscillations rather than static dysbiosis alone. Integrating circadian biology into microbiota research may enable metabolomic stratification and pave the way for precision psychiatry approaches grounded in host–microbe metabolic crosstalk. Future longitudinal and time-resolved multi-omics studies are needed to validate this framework and to translate it into clinically actionable interventions. Full article

Different host plants influence the nutritional and metabolic profiles of the fall webworm (Hyphantria cunea), a globally invasive pest. This study investigated the proximate composition, free amino acid and lipid profiles of its pupae from larvae reared on three distinct diets (Robinia pseudoacacia, Morus alba and Armeniaca sibirica). The results showed that pupal weight and size varied significantly with host plant. The pupae contained 64.94 ± 1.57% crude protein and 30.82 ± 0.53% crude fat (dry mass basis), with high levels of magnesium and calcium. A total of 82 free amino acids and their metabolites were identified, including all essential and non-essential amino acids. In addition, 1026 lipids were detected, with triacylglycerols as the predominant class. Notably, the levels of linoleic and α-linolenic acid were highest in the pupae fed on R. pseudoacacia. Among the three diet groups, the lipid species TG (16:0_16:2_20:5) was identified as a characteristic differential metabolite. These findings show that host-plant-induced nutritional variation reflects metabolic plasticity, which underlies the dietary adaptability and invasion success of this polyphagous pest and also suggestsits potential use as a feed ingredient. Full article

The range of food resources consumed by opportunistic carnivores is shaped by habitat-specific availability and productivity. However, baseline data on the diet of the Japanese weasel (Mustela itatsi) in managed wetland habitats remain scarce. Firstly, we conducted a diet study examining Japanese weasel scats from the Watarase-yusuichi wetland (WYW) (September 2024–August 2025). Based on 103 fecal samples, we calculated seasonal frequency of occurrence (FO) for 16 food categories and estimated their relative volume (RV) using the point-frame method. Surprisingly, plant material and fruit seeds were eaten frequently across seasons, and fruit seeds constituted a major component of scat volume, particularly in summer. Secondly, we compared baseline WYW data with published datasets from two contrasting aquatic habitats (a suburban river area and a rice paddy landscape) using harmonized categories and multivariate analyses. Diet composition differed markedly among study sites, and the PERMANOVA analysis indicated a significant effect of sampling site (R² = 0.643, p = 0.001) with a weaker seasonal effect (R² = 0.208, p = 0.038), with no significant pairwise differences between seasons (all p ≥ 0.300). Although cross-site comparisons should be interpreted cautiously because datasets were collected in different decades (1998, 2018, and 2024–2025), these findings support habitat-associated trophic plasticity in the Japanese weasel, with dietary shifts across habitats and seasons apparently reflecting variation in available food resources. In managed floodplain wetlands such as WYW, maintaining a mosaic of reed beds, ponds, and channels may help sustain dietary flexibility and population persistence in this species. Full article

Physical inactivity contributes to type 2 diabetes (T2D), but the molecular links between exercise and metabolic improvement remain incompletely understood. We meta-analyzed genome-wide association studies of vigorous physical activity and T2D (combined n ≈ 1.95 million) and integrated eQTL/sQTL maps with single-cell and spatial transcriptomic datasets to connect genetic risk with tissues, cell types, and regulatory programs. Tissue and cell-type enrichment, colocalization, and network analyses were performed. Computational findings were further examined in male 10-week-old C57BL/6J mice with high-fat diet-induced diabetes. After 1 week of acclimatization, mice were randomly assigned to normal chow, high-fat diet, or high-fat diet plus exercise groups (n = 6 per group; high-fat diet with 60% of total energy from fat). The exercise intervention consisted of treadmill running (10 m/min for 50 min per day, 5 days per week, total 16 weeks), followed by metabolic phenotyping, skeletal muscle histology, bulk RNA sequencing, alternative splicing analysis, and RT-qPCR of Mau2 isoforms. Exercise- and T2D-associated variants showed joint enrichment in skeletal muscle and adipose eQTL/sQTL signals. Integrated single-cell analyses prioritized fibro-adipogenic progenitors and endothelial cells, and identified an extracellular matrix- and collagen-related module in fibro-adipogenic progenitors associated with both exercise and T2D. Mau2 emerged as a shared candidate gene with tissue-specific splicing signals. In diabetic mice, exercise improved glucose homeostasis and muscle fiber structure, and reduced Mau2 intron retention in skeletal muscle without changing total Mau2 expression. These findings support a multiscale framework linking exercise-responsive regulation to T2D-related tissue remodeling and splicing plasticity. Full article

The brain has a higher energy demand per unit weight than any other organ in the body; however, links between metabolism, diet and neurological function have historically been underexplored. This partly stems from early assumptions that brain metabolism is primarily dependent on glucose and ketone bodies, whereas more recent evidence indicates broader metabolic flexibility and complex cell-type specialisation. In the past few decades, brain metabolism has become increasingly recognised as relevant to neurological and mental health, and many neurodegenerative disorders are accompanied by changes in brain energy utilisation. In parallel, epidemiological studies associate hypercaloric dietary patterns and metabolic disorders—particularly type-2 diabetes mellitus—with increased risk of later cognitive decline and sporadic Alzheimer’s disease, although causal pathways remain difficult to establish in humans. In this narrative review, we summarise selected findings linking “unhealthy” diets to synaptic function, focusing on synaptic plasticity, neuroinflammation and adult hippocampal neurogenesis, and we distinguish between evidence from human observational studies and mechanistic insights from animal and cellular models. We also discuss candidate mechanisms—including insulin resistance-linked signalling changes, lipid-driven inflammatory amplification, oxidative stress, and altered lipid handling—that may contribute to synaptic vulnerability. Finally, we outline translational considerations and key knowledge gaps (including physiological exposure levels and heterogeneity of experimental paradigms) that currently limit inference from preclinical models to clinical intervention. Full article

Plastic-derived chemical additives, including bisphenols, phthalates, perfluoroalkyl substances (PFAS) and microplastic-associated contaminants, are now recognised as widespread environmental toxins that measurably affect endocrine signalling, oxidative balance, inflammation and metabolic homeostasis. Continuous exposure through food contact materials, consumer products, and environmental media raises concerns about long-term health effects. An increasing number of epidemiological and experimental studies are linking these exposures to metabolic disorders, reproductive dysfunction, neurodevelopmental alterations, and increased disease susceptibility throughout the lifespan. This narrative review summarises the latest evidence on the toxicological mechanisms of these compounds, with a focus on endocrine disruption, redox imbalance, reproductive impairment, thyroid hormone dysregulation and epigenetic modifications induced by plastic-derived chemicals. Literature was identified through searches of major scientific databases, including PubMed, Scopus, and Web of Science. Reference screening was also employed to complement these searches and ensure comprehensive coverage of vertebrate and invertebrate models. The inclusion criteria encompassed studies published within the last 10 years, focusing on experimental, experimental, and translational research. The review evaluates phytochemicals such as polyphenols, flavonoids, isoflavones, catechins, sulforaphane, and chlorogenic acid as natural agents that can mitigate the biological effects of plastic-derived toxicants. These compounds exhibit antioxidant, anti-inflammatory, and receptor-modulating properties that counteract pathways disrupted by BPA, phthalates, and PFAS. Experimental studies have demonstrated that phytochemicals can modulate oestrogen receptor activity, enhance detoxification systems, reduce oxidative biomarkers and mitigate epigenetic and metabolic alterations induced by micro- and nanoplastics. Emerging nutritional evidence suggests that diets high in polyphenols may reduce the biological impact of plastic-derived contaminants within the body, rather than reducing exposure itself. This effect appears to be especially relevant during sensitive developmental periods, such as the prenatal, early postnatal and adolescent stages. Full article

Cognition in older adults may be influenced by environmental factors; however, the pathways linking environmental exposures and cognition remain unclear. The aim of this narrative review is to synthesize evidence on the association between the environment and cognition in older adults, integrating biological, environmental, and behavioral elements. Systematic reviews and original studies addressing this topic were identified in Web of Science, PubMed, and Scopus. The primary neural processes associated with maintaining cognition during aging are neuronal plasticity and compensatory scaffolding. Participation in intellectually stimulating activities, physical exercise, and a healthy diet; mitigation of chronic stress; reduction in the severity of depressive symptoms; and buffering against the adverse effects of air pollution are proposed as plausible pathways that may mediate the relationship between neural processes and the environment. In this context, environmental factors that affect cognition can be classified at three levels: (i) micro-level (family and home): social interaction with family members and indoor pollution; (ii) meso-level (community and services): social interaction, land-use diversity, transportation systems, environmental design, and urban green spaces; and (iii) macro-level (society in general and public policies): social representations of old age and aging (positive aging vs. ageism) and public policies aimed at improving pathways related to cognitive maintenance. Overall, the environment may influence cognition in older adults; however, the available studies show methodological and conceptual heterogeneity, inconsistent findings, and important gaps in knowledge. Full article

Microplastic (MP) contamination is increasingly recognized as a global environmental problem affecting aquatic ecosystems, food quality, and animal and human health. Farmed fish represent an important and increasing component of the human diet. Therefore, understanding potential human exposure to MPs is essential for ensuring food safety. In the current paper, we present the results of a preliminary study conducted in Bulgaria on MP contamination in the muscle tissue of rainbow trout [Oncorhynchus mykiss (Walbaum, 1792)] reared in freshwater aquaculture systems. Edible tissues were analyzed using Laser Direct Infrared (LDIR) imaging spectroscopy, a highly sensitive method enabling rapid detection and accurate identification of polymer types present in samples. MPs were detected in all examined specimens, demonstrating that these particles are bioavailable and capable of accumulating in fish muscle tissues commonly consumed by humans. Moreover, the presence of multiple polymer types suggests diverse contamination sources within aquaculture environments. Although the present findings do not allow direct conclusions about human health risks, they indicate potential risks of trophic transfer and highlight the need for improved monitoring strategies and management practices in farmed fish production. Overall, this study provides novel data on MP exposure in aquaculture species and emphasizes the preventive importance of assessing plastic pollution in fish intended for human consumption. Full article

Background: Long noncoding RNAs (lncRNAs) have emerged as critical regulators of hepatic metabolism and disease progression. The hepatocyte nuclear factor 1 alpha antisense 1 (HNF1A-AS1) lncRNA modulates liver-specific transcription factors; however, its physiological role in diet-dependent lipid homeostasis remains poorly defined. Methods: In this study, we investigated the mouse ortholog, Hnf1a opposite strand 1 (Hnf1aos1), using AAV-mediated knockdown in C57BL/6J mice fed either a chow diet (10% kcal from fat) or a high-fat diet (HFD; 60% kcal from fat) for 12 weeks. Metabolic phenotyping included hepatic lipid quantification, histological analysis, serum biochemistry, and quantitative gene expression profiling. Results: Loss of Hnf1aos1 produced distinct, diet-dependent alterations in hepatic lipid handling. Under chow conditions, knockdown mice exhibited selective hepatic cholesterol accumulation (6.10 ± 2.9 mg/g tissue vs. 3.51 ± 1.1 mg/g in controls), accompanied by dysregulation of cholesterol clearance pathways. In contrast, under HFD conditions, knockdown precipitated severe macrovesicular degeneration, with hepatic triglyceride levels approximately doubled relative to HFD-fed controls (51.72 ± 19.8 mg/g vs. 26.34 ± 11.9 mg/g) and a numerically elevated triglyceride-to-cholesterol ratio (TG:TC ≈ 6.1:1; p = 0.0621, trend). Chow/Kd mice gained significantly less weight than chow-fed controls, whereas HFD/Kd mice exhibited weight gain comparable to HFD controls despite severe hepatic steatosis. This paradoxical phenotype suggests impaired metabolic feedback at the post-transcriptional level, in which compensatory upregulation of Hnf1a mRNA is insufficient to suppress lipid-associated genes such as Cd36, despite profound lipid overload; however, HNF1A protein levels were not directly measured in this study. Conclusion: Collectively, these findings identify Hnf1aos1 as a regulator of hepatic lipid homeostasis whose loss produces a phenotype consistent with inappropriate lipid accumulation during nutrient excess, without defining the underlying molecular mechanism. Our results support a role for Hnf1aos1 in shaping hepatic metabolic plasticity and provide insight into lncRNA-associated MASLD phenotypes. Full article

Background/Objectives: Although Drosophila melanogaster is widely used in genetics and nutrition research, developmental kinetics are rarely analyzed using formal mathematical modeling. Most dietary studies present developmental curves without rigorous fitting, limiting quantitative interpretation. This study applies and compares three primary models, as well as develops secondary models, to characterize the effects of high-sugar diets on egg-to-adult (life cycle) development. Methods: Standardized husbandry and an embryo-to-pupa feeding assay were performed across 11 sucrose concentrations. Synchronized embryo collection and high-resolution monitoring were used for this assay. Three primary models—dose–response, Gompertz, and logit-based linearization—were fitted to developmental curves to extract timing (t_mid) and synchrony (s_dvp) parameters. Secondary modeling was used to evaluate how these parameters change with respect to sucrose concentration. Results: Increasing sucrose concentration markedly delayed pupariation and reduced viability at the highest levels. All models showed increasing t_mid and decreasing s_dvp with rising sugar concentration, with the Gompertz model providing the best overall performance. Secondary modeling revealed a consistent bilinear response with a breakpoint at 0.52–0.62 M, separating low-, medium-, and high-sucrose conditions. Reduced sampling frequency decreased model robustness, while twice-daily observations remained sufficient. Conclusions: Mathematical modeling provides a robust, practical framework for quantifying the effects of diet on D. melanogaster development. The Gompertz model provided the best fit and yielded biologically interpretable parameters. The bilinear secondary model effectively captured sucrose-dependent stress responses and quantified plasticity through environment-dependent changes in developmental timing and synchrony. Overall, this work establishes a quantitative practical framework for modeling developmental kinetics under nutritional perturbations, and the approach can be extended with additional secondary environmental factors to improve predictive analyses of nutritional effects. Full article

The present study aimed to investigate the effects of polyvinyl chloride microplastics with different sizes on the growth, intestinal and hepatic health of turbot (Scophthalmus maximus L.) at 3 and 9 weeks of exposure. Three diets were formulated: a control diet with no microplastics, a diet containing 2% micrometer-sized plastics (MPs), and a diet containing 2% nanoplastics (NPs), with four replicates (40 fish/tank, 12 tanks total). The results showed that MPs and NPs had no significant effects on the growth performance of turbot. Analyses of intestinal histology and gene expression (intestinal barrier-related and antioxidant-related genes) indicated that the turbot intestine exhibited a certain degree of tolerance and adaptability to MPs and NPs exposure. Observations of liver histology and analyses of gene expression (inflammatory cytokines, apoptosis-related, and antioxidant-related genes) revealed that the liver damage induced by microplastics in turbot exhibited obvious size-dependent and time-cumulative effects, with NPs exerting a stronger impact. Compared with MPs, long-term exposure to NPs can induce obvious intestinal microbiota dysbiosis in turbot. In summary, particle size and exposure duration are important factors regulating the impacts of PVC microplastics on the intestinal and hepatic health of turbot. Full article

Longevity in the olive fruit fly, Bactrocera oleae, is a plastic trait shaped by the synergistic interaction between reproductive effort, sex, and protein availability. This study investigated how the survival of 800 individuals is affected by protein limitation and mating status. Results from Cox proportional hazards analysis demonstrate that mating and protein deprivation significantly increase mortality risk. Under protein-deprived conditions, mating increased the mortality hazard by 146.5% for males and 121.5% for females compared to virgins. Notably, a significant Sex × Diet interaction (p = 0.022) confirmed that among virgin individuals, the relative mortality hazard increase under protein scarcity was nearly double for males (97.5%) compared to females (51.1%), indicating a higher statistical tolerance for nutritional stress in females. Furthermore, statistical validation confirmed that diet exhibited a significant time-dependent effect (p = 0.029), indicating that nutritional deficits act cumulatively over the fly’s lifespan. These findings suggest that B. oleae longevity is governed by dynamic, synergistic pressures, with females exhibiting a lower hazard of death under resource-limited conditions, an insight essential for refining demographic models in integrated pest management (IPM) strategies. Full article

Adult neurogenesis, the process of generating new, functional neurons in the mature central nervous system, represents a key mechanism of brain plasticity and a potential source of regeneration. This process occurs primarily within specialised neurogenic niches: the subgranular zone of the hippocampal dentate gyrus (SGZ) and the subependymal zone (SEZ). It is regulated by a complex network of endogenous factors (e.g., hormones, neurotrophins, growth factors) and exogenous factors (environment, stress, diet, physical activity). Impairments in neurogenesis are linked to the pathogenesis of neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). In their course, chronic inflammation, mitochondrial dysfunction, oxidative stress, and the accumulation of pathological proteins (β-amyloid, Tau protein, α-synuclein) create a microenvironment that inhibits the proliferation, differentiation, and survival of new neurons. This results in the exacerbation of cognitive and memory deficits. A review of the literature indicates that modulating neurogenesis through non-pharmacological interventions (e.g., a diet rich in anti-inflammatory compounds, physical exercise) and targeted therapeutic strategies represents a promising, albeit complex, research avenue. The primary challenge remains not only stimulating neuron generation but also ensuring their proper maturation, survival, and functional integration into existing neuronal circuits. A deeper understanding of the molecular and environmental mechanisms regulating adult neurogenesis may open new therapeutic possibilities for slowing the progression of neurodegenerative diseases. Full article