Search Results (5,381)

Background: The Taiwanese loach (Paramisgurnus dabryanus ssp. Taiwan, Dabry de Thiersant, 1872.) is an economically important aquaculture species in East Asia, and its body color directly affects its ornamental and market value. Our research group recently discovered a golden-red mutant, named “Gan Hong No. 1” (MR), within a wild-type (WT) population. During embryogenesis, MR individuals exhibit almost no melanophore deposition, and after hatching, xanthophores and erythrophores appear sequentially, suggesting that the body color variation likely originates from alterations in the gene regulatory network during early development. Objective: To systematically compare the transcriptomes of WT and MR-Taiwanese loach during early development, to identify the key regulatory pathways underlying red body color formation from a temporal perspective, to test whether the classical melanin synthesis pathway is impaired, and to provide a theoretical basis for selective breeding of body color traits. Methods: High-throughput transcriptome sequencing was performed on eight early developmental stages (0, 5, 10, 15, 20, 23, 28 and 43 h post-fertilization) of both loach types. Differential expression analysis, time-series trend analysis, and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment were used to systematically characterize gene expression dynamics. Transcriptomic data validation was performed using real-time PCR. Results: In MR, the core transcription factor mitfa was significantly downregulated, whereas the expression of melanin synthesis genes such as kita and dct showed no significant difference, indicating that the impairment of melanogenesis is caused by mitfa downregulation. Trend analysis and pathway enrichment revealed that in MR embryos, pathways related to oxidative stress, unsaturated fatty acid biosynthesis, C-type lectin receptor signaling, p53 signaling, and apoptosis were significantly activated, while the thyroid hormone synthesis pathway was markedly upregulated. In WT, these pathways showed the opposite trend. qRT-PCR results were consistent with the transcriptome data. Conclusions: This study demonstrates that downregulation of mitfa serves as the initial trigger for red body color variation in the Taiwanese loach. This mutation impedes melanin synthesis and concurrently activates a coordinated regulatory network involving oxidative stress, immune inflammation, and thyroid hormone signaling. Accumulation of unsaturated fatty acids alleviates oxidative damage and supports carotenoid deposition, while immune signals eliminate aberrant melanocytes and promote compensatory generation of red and yellow chromatophores. The upregulated thyroid hormone further fine-tunes pigment cell differentiation. For the first time in a cobitid species, this study elucidates the mitfa-mediated, multi-pathway synergistic molecular mechanism driving the transition from melanin-based to carotenoid/pteridine-based red coloration in fish, thereby providing a theoretical reference for molecular breeding of body color in aquaculture. Full article

Background: Renal ischemia–reperfusion injury (RIRI) is a major cause of acute kidney injury (AKI) and contributes to delayed graft function and progression toward chronic kidney disease. In addition to oxidative stress and inflammation, RIRI induces profound metabolic derangements, particularly suppression of tubular fatty-acid β-oxidation (FAO), leading to energetic stress, lipid accumulation, and maladaptive repair. Peroxisome proliferator–activated receptor-α (PPARα) is a key regulator of tubular FAO, but whether Schisandrin B (Sch B) mitigates RIRI through restoration of a PPARα-associated metabolic program remains unclear. Objective: To determine whether Sch B alleviates RIRI in association with restoration of tubular FAO and attenuation of lipid accumulation and fibrotic remodeling. Methods: A unilateral murine renal I/R model and an HK-2 hypoxia/reoxygenation (H/R) model were used. Mice received Sch B (20 or 40 mg/kg/day) before I/R, and a subset was co-treated with the PPARα antagonist GW6471. Renal function, tubular injury, fibrosis, lipid accumulation, and FAO-related proteins were assessed by serum biochemistry, histopathology, Oil Red O staining, transmission electron microscopy, immunohistochemistry, immunofluorescence, and Western blotting. Bulk RNA-seq and public single-cell RNA-seq datasets were integrated to characterize metabolic pathway remodeling and cell-type-associated PPARα changes. Molecular docking and molecular dynamics simulations were performed to explore the potential interaction between Sch B and PPARα. Results: Sch B significantly improved renal function, reduced tubular injury, and attenuated interstitial collagen deposition after I/R. Sch B also reduced lipid droplet accumulation, preserved mitochondrial ultrastructure, and restored the expression of FAO-related proteins, including CPT1A, CPT2, and ACADM. In vivo and in vitro, Sch B decreased α-SMA, COL1A1, and vimentin expression, indicating attenuation of EMT-associated/profibrotic remodeling. Integrated transcriptomic analyses supported marked metabolic reprogramming after I/R, with enrichment of FAO- and PPAR-related pathways and reduced PPARα expression predominantly in tubular compartments. Sch B was associated with restoration of tubular PPARα expression, while docking and molecular dynamics analyses supported a plausible Sch B–PPARα interaction in silico. GW6471 blunted the beneficial effects of Sch B on fibrosis-related and FAO-related readouts. Conclusions: Sch B alleviates RIRI and limits subsequent fibrotic remodeling in association with restoration of a PPARα-related tubular FAO program, reduced lipid accumulation, and preservation of tubular metabolic homeostasis. These findings identify metabolic reprogramming as an important component of Sch B-mediated renoprotection, although the precise mode by which Sch B regulates PPARα requires further investigation. Full article

Background: Platinum-based chemotherapy is the frontline treatment for high-grade serous ovarian cancer (HGSOC); however, the development of therapy resistance greatly limits clinical response. Increasing evidence suggests that platinum agent-driven metabolic programming, particularly within redox-associated pathways, may contribute to chemoresistance. Methods: A syngeneic pair of patient-derived HGSOC cell lines representing cisplatin-sensitive (SE) and cisplatin-resistant (CR) states were evaluated using a multi-omics approach. Differential metabolite abundance and gene expression were assessed, followed by gene set and pathway enrichment analyses to identify coordinated metabolic shifts. In silico analysis of an additional sensitive and resistant HGSOC cell line validated the glutathione pathway upregulation seen in the patient-derived model. The functional contribution of the glutathione pathway on cisplatin resistance was evaluated following glutathione inhibition. Results: Chronic cisplatin exposure induced extensive metabolic rewiring in CR cells, characterized by enrichment of glutathione metabolism at both the metabolite and gene levels. Increased reduced glutathione was observed alongside upregulation of key enzymes involved in its de novo biosynthesis, recycling, and utilization, consistent with enhanced detoxification capacity relating to cisplatin-induced oxidative stress. Additionally, taurine was highly enriched, further highlighting a metabolic shift towards enhanced antioxidant mechanisms. CR cells also demonstrated an increase in NADPH-generating pathways, including amino acid metabolism and fatty acid β oxidation, to support redox balance and biosynthetic demands of increased glutathione metabolism. Transcriptional remodeling of the γ-glutamyl cycle further indicated a shift toward increased glutathione turnover, suggesting that the coordinated changes seen may define a metabolic state enhanced in oxidative stress tolerance and therapeutic resistance. These transcriptional changes were also seen in another model of platinum sensitivity/resistance, indicating a conserved response associated with platinum-induced resistance. Finally, concurrent cisplatin treatment and glutathione inhibition significantly increased sensitivity within the CR cells. Conclusions: These findings suggest that cisplatin-resistant cells, previously exposed to a platinum-based agent, may undergo distinct metabolic rewiring towards antioxidant pathways to survive chronic chemotherapeutic stress. Targeting components of these systems may represent a viable strategy to overcome platinum resistance and improve therapeutic outcomes. Full article

Chicken meat palatability is shaped by what the meat contains (e.g., intramuscular fat and fatty-acid composition), what happens to those components during storage and cooking (including oxidation and transfer into soups or meat juices), and how tastebud signaling integrates the resulting stimuli. Chicken sold in Japan as “Jidori” (premium native-line products) is often described as having a richer flavor that lingers longer than that of standard broiler chicken, and published poultry work, including reports by the author and their colleagues, has linked this phenotype to higher arachidonic acid (AA) levels in the meat; however, the mechanistic basis remains under debate and has not been overturned. In addition, intact AA is a highly hydrophobic long-chain fatty acid that partitions poorly into aqueous phases, making a direct “AA-as-tastant” mechanism unlikely. This review develops a hierarchical interpretation that separates food-level associations from tastebud mechanisms and reframes AA as a primarily downstream lipid substrate. Two complementary routes are proposed: (i) a food-chemistry route in which cooking and storage oxidation generate low-molecular-weight, water-accessible lipid-oxidation products that partition into soups, meat juices, and cooking loss, and (ii) a receptor-centered route in which kokumi-related signaling pathways, particularly those involving the calcium-sensing receptor (CaSR), amplify taste intensity, continuity, and aftertaste within tastebuds. This framework emphasizes how these routes can be linked experimentally by combining matrix/phase manipulations with targeted carbonyl profiling, fractionation–reconstitution, and pathway-perturbation assays in tastebud readouts. Overall, the model is intended to support mechanism-focused study designs beyond single-compound explanations. Full article

The transition to bio-based fuels requires a thorough understanding of how molecular structure governs key physicochemical properties such as oxidation stability and viscosity. In this study, the combined influence of fatty acid composition and alcohol structure on biodiesel and biolubricant performance is investigated using a multivariate statistical approach. A dataset comprising 108 samples was analyzed, including 17 experimental samples produced in this work and 91 samples collected from peer-reviewed literature. Each sample was characterized by its fatty acid composition and at least one physicochemical property, namely oxidation stability (Rancimat induction time) and/or kinematic viscosity. Principal Component Analysis (PCA) was applied to identify dominant compositional patterns, followed by clustering (k-means) to define homogeneous compositional regions. Within these regions, a variance decomposition approach was used to quantify the relative contribution of alcohol type to property variability. The results show that fatty acid composition defines the primary structural framework governing oxidative stability, largely driven by the degree of unsaturation. In contrast, viscosity is more strongly influenced by the type of alcohol used, particularly in systems involving higher alcohols or polyols. The proposed approach provides a structured multivariate framework focused on analyzing oxidation stability and viscosity, enabling the systematic interpretation of the relative influence of fatty acid composition and alcohol structure on these key physicochemical properties. This study demonstrates that integrating PCA, clustering, and variance decomposition offers a robust strategy for analyzing complex bio-based systems, supporting the rational selection of feedstocks and processing conditions for the optimization of biodiesel and biolubricant formulations. Full article

Dandruff (DF) is a prevalent, recurrent inflammatory scalp disorder increasingly recognized as a complex state of functional dysbiosis rather than a simple Malassezia overcolonization. The scalp microbiome is predominantly shaped by Malassezia species (M. restricta and M. globosa), Cutibacterium, and Staphylococcus species. Recent multi-omics evidence indicates that DF pathogenesis is driven by the destabilization of microbial interaction networks and strain-level functional heterogeneity, characterized by the disruption of the C. acnes/S. epidermidis balance and the opportunistic expansion of Staphylococcus aureus. Mechanistically, Malassezia utilizes its lipolytic repertoire to hydrolyze host sebum into irritant free fatty acids and peroxides. Concurrently, oxidative metabolites like squalene peroxide (SQOOH) penetrate the stratum corneum to activate the NF-κB and aryl hydrocarbon receptor (AhR) pathways, triggering a pro-inflammatory cascade that overexpresses keratins (K6/16/17) and downregulates filaggrin. This molecular cascade drives abnormal keratinocyte turnover and lipidomic remodeling, establishing a self-perpetuating “metabolism–inflammation–barrier disruption” pathological cycle. This review systematically elucidates the molecular etiology of DF as an ecological disorder driven by a tripartite imbalance among the microbiome, host physiology, and the environmental niche. We propose that next-generation therapeutic paradigms must transcend traditional antifungal eradication, focusing instead on targeted molecular intervention and microecological restoration to recalibrate overall scalp homeostasis. Full article

Oleogels have emerged as promising alternatives to conventional solid fats by structuring liquid oils without increasing trans or saturated fat levels. This study therefore aimed to develop rice bran oil (RBO)-based oleogels using beeswax (BW), carnauba wax (CW), and their combinations, and to compare their physicochemical properties with commercial margarine. Thirteen formulations with varying wax concentrations were prepared and analyzed using differential scanning calorimetry, microscopy, rheology, texture profile analysis, oil binding capacity, slip melting point, peroxide value, color analysis, and fatty acid profiling. Our results demonstrated that the thermal behavior of the oleogels is dependent on the type and concentration of the wax, with CW oleogels exhibiting higher crystallization and melting temperatures than BW, while hybrid systems displayed intermediate and synergistic properties. Distinct crystal morphologies were observed, with BW forming needle-like and CW forming spherulitic structures, while the hybrids created interconnected networks. All samples exhibited shear-thinning and gel-like behavior, with greater viscosity and gel strength observed at increasing wax concentrations. The hybrid oleogels achieved hardness comparable to higher CW levels and approached margarine texture, while maintaining high oil binding capacity (>94%). The RBO oleogels contained higher unsaturated fatty acids but showed lower oxidative stability than margarine. Overall, BW–CW hybrid oleogels demonstrated strong potential as healthier, solid fat alternatives with improved structural and thermal characteristics. Full article

Salmonella primarily affects the gastrointestinal tract, causing local and systemic symptoms. Fucoidan exhibits therapeutic potential against Salmonella-induced pathology; however, the influence of its molecular weight on efficacy remains poorly understood. In this study, low-molecular-weight fucoidan from Undaria pinnatifida (LUPF) was prepared and characterized, and its protective effects against Salmonella infection were evaluated in a mouse model. LUPF effectively mitigated Salmonella-induced multiple organ damage by preserving mucin secretion and tight junction protein expression. Metabolomics analysis further demonstrated that LUPF normalized Salmonella-induced metabolic disturbances, thereby reducing systemic dysfunction. Mechanistically, LUPF suppressed inflammation by inhibiting mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling pathways, while alleviating oxidative stress through activation of the Nrf2 pathway. In addition, LUPF restored gut microbiota homeostasis by reducing Proteobacteria levels, improving the Bacteroidota/Firmicutes ratio, enriching beneficial taxa, and enhancing short-chain fatty acid production. In vitro experiments further revealed that LUPF attenuated Salmonella-induced inflammation by modulating macrophage polarization. Collectively, these results suggest that LUPF has promising potential as a prebiotic candidate for reducing the risk of Salmonella-associated diseases. Full article

Background/Objectives: Age-related functional decline is increasingly linked to chronic low-grade inflammation (inflammaging) and sarcopenia, two interconnected processes contributing to frailty, metabolic dysregulation, and impaired physical function. These conditions share several underlying mechanisms, including immune dysregulation, mitochondrial dysfunction, oxidative stress, and impaired anabolic signaling. This narrative review critically evaluated the mechanistic and translational interactions between natural bioactive compounds and lifestyle interventions in modulating inflammaging and sarcopenia. Methods: Evidence from molecular, experimental, epidemiological, and clinical studies was synthesized to examine the effects of bioactive compounds—including polyphenols, flavonoids, carotenoids, and omega-3 fatty acids—as well as physical activity and dietary patterns. Particular emphasis was placed on inflammatory regulation, redox homeostasis, mitochondrial adaptation, and muscle metabolism, including NF-κB, AMPK–mTOR, and Nrf2 signaling pathways. Results: Observational studies and randomized controlled trials generally indicate that anti-inflammatory dietary patterns and regular physical activity are associated with improved muscle strength, physical performance, and inflammatory status in older adults. Mechanistically, nutritional bioactives and exercise appear to converge on several pathways involved in mitochondrial function, oxidative stress, anabolic signaling, and immune activation. Emerging evidence suggests potential convergence and interaction of biological pathways affected by nutritional and lifestyle interventions; however, formal evidence demonstrating true synergistic effects in humans remains limited. Nevertheless, substantial heterogeneity persists regarding intervention protocols, dosage strategies, bioavailability, and long-term clinical outcomes. Conclusions: Natural bioactive compounds and lifestyle-based interventions represent promising approaches for targeting biological processes implicated in inflammaging and sarcopenia. By integrating current evidence within a hormesis-oriented geroscience framework, this review highlights the importance of adaptive redox regulation, metabolic resilience, and evidence-based lifestyle strategies in healthy aging. Future well-designed longitudinal and intervention studies are needed to clarify the clinical relevance of these interactions and optimize translational implementation. Full article

Hantaviruses (HTVs) are lethal zoonotic pathogens responsible for hemorrhagic fever with renal syndrome and HTV cardiopulmonary syndrome; however, no specific antiviral treatments or vaccines have been approved. Bee products, such as propolis, honey, royal jelly, bee venom, and bee pollen, demonstrate extensive antiviral, anti-inflammatory, antioxidant, and immunomodulatory properties against various RNA and DNA viruses. No published research has directly evaluated bee products in relation to HTV infection. This review proposes a hypothesis-driven mechanistic framework suggesting that bioactive compounds from bee products may concurrently inhibit HTV replication, alleviate the cytokine storm, diminish oxidative stress, and maintain endothelial barrier integrity. We explicitly recognize the lack of direct experimental evidence regarding bee products’ efficacy against HTVs. Considering the mechanistic similarities with other enveloped viral infections and the recognized functions of NF-κB, Nrf2, and endothelial signaling pathways in HTV pathogenesis, we present a scientifically substantiated rationale for forthcoming research endeavors. The diverse bioactive compounds present in bee products including bee pollen, bee venom, honey, propolis, and royal jelly could provide a multifaceted strategy for inhibiting HTV pathology. We propose systematic in vitro, in silico, and in vivo investigations to assess the potential of bee-derived flavonoids, peptides, and fatty acids as adjunctive therapeutic strategies for HTV disease. Full article

Introduction: Lutein+Zeaxanthin (L+Z) are the major constituents of macular pigments of the retina. There is a lack of information on the bioavailability of the two compounds in the presence and absence of omega-3 fatty acids in L+Z supplements which are commonly prescribed to treat macular degeneration. Despite growing interest in L+Z supplementation, there remains a limited understanding of their short-term bioavailability dynamics and the potential added value of omega-3 co-supplementation. This pilot study reports on the bioavailability of serum responses to L+Z supplements in the presence of omega-3 fatty acids and evaluates time-resolved analytical approaches using Area Under the Curve. Subjects/Methods: A total of 10 men and six women with an average age of 31.38 ± 1.27 years participated in this randomised, non-blinded, controlled study for a total of 19 days (7-day wash-out period plus 12-day intervention period). The control group (n = 9) consumed the L+Z supplement (12 mg/d) only, while the intervention group (n = 7) consumed the L+Z supplement along with 900 mg/d of an omega-3 supplement (540 mg EPA + DHA 360 mg). Each group adhered to a comprehensive low-carotenoid and omega-3 diet list (LCOD) for the 7-day wash-out period and the 12-day intervention period. The participants reported the foods they consumed daily in their diet logbooks, online logs, and the ASA 24 diet assessment log over the study period. The body composition of each subject in the two groups was assessed before and after the study using a SECA body composition analyser, and the relative serum L+Z response in both groups was determined using Area Under the Curve (AUC and incremental AUC) by trapezoidal approximation. Results: The mean ± SEM baseline serum lutein+zeaxanthin (L+Z) concentrations measured at the end of the wash-out period (Day 7) were 2.23 ± 0.65 µg/mL in the control group and 1.20 ± 0.53 µg/mL in the intervention group. Following wash-out, serum L+Z concentrations increased in both groups, reaching 2.81 ± 0.90 µg/mL (control) and 2.63 ± 1.21 µg/mL (intervention) at Day 13, and 2.98 ± 0.69 µg/mL (control) and 3.02 µg/mL (intervention) at Day 19. Total exposure assessed by AUC₇–₁₃ and AUC₁₃–₁₉ did not differ significantly between the groups (p > 0.05). Incremental exposure analyses identified the post-wash-out period as the primary biologically responsive window, with higher mean incremental L+Z bioavailability in the intervention group (4.36 µg/day/mL) compared with the control group (3.00 µg/day/mL), although this difference was not statistically significant (p > 0.05). No significant effect of omega-3 co-supplementation on oxidative stress biomarkers was observed (p > 0.05). Conclusion: Omega-3 co-supplementation did not demonstrate a consistent additional benefit on L+Z bioavailability or oxidative stress markers. Day-resolved analyses using iAUC revealed temporal patterns not captured by conventional AUC measures. These exploratory findings should be interpreted with caution and confirmed in larger, longer-term studies. Full article

Sesame is a considerable oilseed crop, but its growth and production are restricted by drought. Potassium (K) is well known for its mitigating effects against drought. Here, two consecutive years of experiments were conducted with varying K fertilizer rates (0, 60, and 120 kg K₂O ha⁻¹) under well-watered and drought conditions to evaluate the impacts of K on sesame seed quality. The results demonstrated that, compared to well-watered conditions, drought caused a decline in seed oil content (5.9–8.6%) but inversely induced an increase in seed K (8.5–23.8%), lignans (10.2–21.6%), and essential amino acids over a period of 2 years. Potassic fertilizer significantly increased seed K, oil, and lignans contents, aligning with ameliorative oil and protein yield relative to K deficiency plants under drought. Moreover, K supply (especially 120 kg K₂O ha⁻¹) increased proline and tryptophan contents by 5.2% and 4.9% under drought compared to the plants without K application, which contributed to producing lignans and enhancing the capacity against oxidative changes. Under drought, 60 and 120 kg K₂O ha⁻¹ application significantly increased linoleic (5.5–9.3%), and stearic acids (7.1–13.7%) content while decreasing palmitic (5.3–14.7%), oleic (4.6–6.4%), and linolenic acids (4.8–11.9%) content, respectively, thereby increasing the ratio of unsaturated to saturated fatty acids and unsaturation index compared with control without K. Overall, K application at the rate of 120 kg K₂O ha⁻¹ could be considered as a practical and straightforward strategy to improve the quality of sesame seed products by increasing seed K, oil, lignans, linoleic acid, and unsaturated index for pharmaceutical and food purposes in areas encountering drought stress. Full article

Lipid peroxidation (LPO) is a process where polyunsaturated fatty acids (PUFA) in cellular membranes are oxidized. This process is mediated by reactive oxygen species (ROS) and leads to the formation of reactive products, including 4-hydroxynonenal (4-HNE), malondialdehyde (MDA), and oxidized phospholipids. At low concentrations these products act as second messengers in adaptive redox signalling and metabolic homeostasis, whereas at higher concentrations they compromise membrane integrity and promote cell death. Lipid peroxidation plays a crucial role in anticancer therapies. Here we focus on three mechanistically complementary drugs—sorafenib, cisplatin, and olaparib—because each converges, directly or indirectly, on the redox/LPO axis (system xc−/GPX4 modulation, mitochondrial ROS, and SLC7A11 regulation, respectively), modulating tumor cell responses by inducing PUFA oxidation, mitochondrial dysfunction, and membrane damage. However, tumor cells have several protective pathways against oxidative stress, such as increased expression of glutathione peroxidase 4 (GPX4), the SLC7A11 system Xc, and detoxification of reactive aldehydes. Enrichment of membranes with PUFA increases susceptibility to lipid peroxidation and ferroptosis, thereby sensitizing tumor cells to therapy, whereas enrichment with monounsaturated fatty acids (MUFA), driven by the SREBP1–SCD1 axis, limits peroxidation and confers resistance. Among regulated cell death modalities, ferroptosis is strictly dependent on lipid peroxidation, whereas apoptosis, necrosis, necroptosis, pyroptosis, and immunogenic cell death can be modulated by lipid peroxidation but do not universally require it. Collectively, these mechanisms indicate that lipid peroxidation is an important—though not exclusive—determinant of anticancer drug sensitivity and resistance, and that its dual, context-dependent role (tumor-suppressive at high flux, tumor-promoting under chronic, sub-lethal exposure) must be considered when designing LPO-based therapeutic strategies. Full article

Heat stress leads to excessive hepatic lipid deposition and oxidative imbalance in laying hens, especially during peak laying period. Chlorogenic acid (CGA), a dietary polyphenol with antioxidant and lipid-modulating properties, may improve hepatic lipid homeostasis, yet its effects under heat-stress conditions remain unclear. In this study, 240 Hy-Line Brown laying hens at 36 weeks of age were randomly assigned to one of two treatments (120 hens per treatment, with six replicates of 20 hens each): a basal diet or a basal diet supplemented with 300 mg/kg CGA and subjected to heat-stress conditions for 8 weeks. CGA supplementation significantly reduced liver weight (25.3%), liver index (14.4%), hepatic triglyceride content (29.1%), and serum triglyceride level (61.7%) (p < 0.05). Histological assessment revealed lower steatosis and inflammation scores, alongside increased hepatic SOD activity (13.6%) and decreased MDA content (58.7%) (p < 0.05). RNA-seq analysis identified 420 differentially expressed genes that were significantly enriched in PPAR signaling and fatty acid β-oxidation pathways. CGA upregulated fatty acid oxidation-related genes (ACSL1, CPT1A, ACOX1, ACAA1) and downregulated lipogenic markers (FASN, ACACA). Serum metabolomics revealed coordinated changes in lipid and carbon metabolism. These results indicate that dietary CGA alleviates hepatic lipid accumulation and oxidative stress in heat-stressed peak-laying hens, potentially via PPARα-mediated enhancement of fatty acid oxidation and inhibition of de novo lipogenesis. Full article

Canned fish products enable long-term preservation of fish, a vital source of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Despite research on lipid composition, gaps remain in understanding the bidirectional fatty acid (FA) exchange between fish muscle and coating media during processing and storage. After a systematic literature search across five databases (PubMed, Scopus, Web of Science, Wiley Online Library, Cochrane Library), 20 studies were included examining FA profiles across fish species, filling media (vegetable oils, brine, tomato sauce), and storage durations (up to 5 years). Five studies showed that n-3 FAs migrate from fish to the filling medium, enhancing its nutritional value, while fish muscle absorbs FAs from the oil, increasingly resembling the filling medium. The use of n-6 FA-rich oils (sunflower, soybean) lowered the n-3/n-6 ratio in flesh. Conversely, aqueous media (brine) and tomato sauce maintained better ratios. EPA and DHA content generally decreased due to canning and storage, with retention varying by fish species, filling medium, and sterilization method. This review underscores significant FA exchange between fish and filling media, confirming bidirectional lipid interchange during processing. To optimize health benefits, aqueous packing media are recommended to preserve lipid profiles or to consume the covering oil to recover nutrients. Further research is needed on other factors altering FA content in canned fish such as environmental and geographical variables (including catching season), pre-canning preparation and sterilization steps (such as freezing, steaming, and frying), sterilization conditions (time, temperature, F₀ value) and lipid oxidation induced by thermal processing. Full article