Search Results (253)

This study evaluated the efficacy of post-extraction American cockroach (Periplaneta americana) residue (PAR) as a dietary feed ingredient on the growth performance, antioxidant defense, and whole-body amino acid profile of juvenile black carp (Mylopharyngodon piceus). A total of 300 juvenile black carp (initial weight 17.19 ± 0.20 g) were fed five isonitrogenous and isolipidic diets for 64 days. PAR was supplemented at inclusion levels of 0% (control), 5%, 10%, 15%, and 20% (corresponding to progressive reductions in dietary fishmeal). The results showed that fish fed the diet with 5% PAR inclusion maintained growth performance and feed conversion efficiency comparable to those of the control group (p > 0.05). Thus, 5% PAR did not significantly improve growth performance, but it did not impair growth under the present experimental conditions. Moreover, 5% PAR supplementation significantly increased hepatic catalase activity and was associated with numerically higher values of several other antioxidant- and immune-related indices. PAR inclusion also increased whole-body glycine deposition, whereas high inclusion levels reduced whole-body methionine content and crude protein deposition. Dietary PAR inclusion at higher levels, especially 20%, was associated with a possible reduction in feed utilization, altered organ indices, altered serum glucose levels, suppressed hepatic transaminase activities, and changes in digestive enzyme activities. However, these responses should be interpreted as the combined outcome of ingredient substitution, amino acid imbalance, altered lipid source, possible essential fatty acid changes, chitin/fiber-like fractions, and metabolic burden, rather than as effects of chitin alone. In conclusion, 5% PAR may be a suitable practical inclusion level for juvenile black carp under the present experimental conditions, whereas excessive inclusion should be used with caution and may require amino acid balancing, improved processing, and further evaluation of dietary gross energy, fatty acid profile, and chitin content. Full article

This study integrated an in vivo feeding trial (0.00–1.00% choline chloride) with in vitro primary hepatocyte experiments to elucidate the molecular mechanisms by which choline chloride alleviates hepatic lipid deposition in bighead carp. The results showed that dietary supplementation with 0.80–1.00% choline chloride significantly reduced hepatic triglyceride (TG) content and lipid droplet accumulation. At the molecular level, choline markedly downregulated lipogenic genes (g6pd, accα, fas) while upregulating genes involved in lipolysis (cpt1α, acox1) and lipid transport (apob-100, mttp). Non-targeted lipidomics revealed that choline maintains lipid homeostasis primarily via the glycerophospholipid metabolism pathway, significantly increasing levels of phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylserine (PS). Furthermore, choline intervention enhanced the expression of its own metabolism-related genes (slc44a2, chdh, ck, chpt1), accelerating choline transport and phosphorylation. Overall, based on the results of this experiment, 0.80% is the recommended supplemental level of choline chloride in diets, which can effectively alleviate lipid deposition in bighead carp. The mechanism involves inhibiting lipogenesis and promoting lipid decomposition and transport through glycerophospholipid pathways, while simultaneously enhancing PC synthesis to accelerate hepatic lipid export. These findings provide a theoretical basis for precise feed formulation in bighead carp. Full article

To investigate the effects of mulberry leaf extract (MLE) on the growth performance, organ indices, and flesh quality of grass carp (Ctenopharyngodon idella), a basal diet (Control, Crude protein 30.25%, Crude lipid 7.23%) and three MLE-supplemented diets containing 1%, 2%, and 4% MLE (MLE1%, MLE2%, MLE4%) were formulated. A total of 160 grass carp (259.7 ± 1.1 g) were randomly allocated into 16 cages (1 m × 1 m × 1.2 m), with 10 fish per cage and 4 replicate cages per treatment group. Throughout the 8-week feeding trial, juvenile grass carp were fed three times daily (08:00, 12:00, and 17:00) at a daily feeding rate of 1.5–2.0% body weight. At the end of the trial, growth performance was assessed. Additionally, four fish were randomly sampled from each cage to determine the organ indices, flesh quality parameters, and gene expression levels. In the results, the final average body weight of all groups ranged from 909.00 to 942.97 g, and all the groups exhibited no significant difference in growth performance (p > 0.05). MLE-supplemented groups had significantly decreased visceral somatic index and hepatic somatic index (p < 0.05). In terms of flesh quality, all MLE-supplemented groups increased the flesh shear force, springiness, whiteness, and lightness (p < 0.05). Compared with the Control group, the MLE4% group had increased flesh hardness, gumminess, and chewiness, from 2899.52 g, 1310.62, and 516.59 to 4122.99 g, 1958.48, and 887.76, respectively (p < 0.05). MLE significantly decreased the 48 h thawing loss (MLE2%), 96 h thawing loss (MLE1%, MLE2%, MLE4%), and flesh crude lipid content (MLE2%, MLE4%) (p < 0.05). In terms of collagen metabolism, compared with the Control group, MLE significantly increased the flesh collagen content (MLE2% and MLE4%) (p < 0.05), upregulated the expression level of La ribonucleoprotein 6 (MLE4%) and tissue inhibitor of metalloproteinase 1 (MLE4%). Matrix metallopeptidase 2 was significantly downregulated in all MLE-supplemented groups (p < 0.05). In terms of myofiber development, compared with the Control group, the myofiber density was higher, and the myofiber diameter was lower in all MLE-supplemented groups (p < 0.05). MLE significantly upregulated the expression level of mammalian target of rapamycin (MLE4%), musculoskeletal embryonic nuclear protein 1 (MLE4%), myogenic differentiation 1 (MLE2%, MLE4%), and myogenic factor 5 (MLE1%, MLE2%, MLE4%) (p < 0.05). Myotubularin-related protein 8 was significantly downregulated in all MLE–supplemented groups (p < 0.05). In conclusion, dietary supplementation with 2–4% MLE improves the flesh textural properties, chroma and water-holding capacity of grass carp. MLE improves the flesh quality of grass carp by enhancing collagen deposition and myofiber development. Full article

Background/Objectives: As obesity continues to increase globally, it has become a major contributor to the growing burden of metabolic diseases, including type 2 diabetes mellitus, cardiovascular disease, and nonalcoholic fatty liver disease (NAFLD). Hepatic lipid accumulation during obesity contributes to oxidative stress and alterations in mitochondrial homeostasis, key features of NAFLD progression. This study investigated whether vitamin D insufficiency aggravates obesity-related hepatic steatosis in association with changes in hepatic sirtuin 1 (SIRT1) activity and nuclear factor erythroid 2–related factor 2 (Nrf2)-related antioxidant gene expression. Methods: Male C57BL/6J mice were maintained on one of three dietary regimens for 16 weeks: a normal diet (NOR; 10% fat containing 1000 IU vitamin D/kg), a high-fat diet (HF; 60% fat containing 1000 IU vitamin D/kg), or a vitamin D-deficient high-fat diet (HF + NVD; 60% fat with no added vitamin D). Results: Vitamin D insufficiency in HF-fed mice (HF + NVD) was associated with significantly higher hepatic triglyceride accumulation and lipid peroxidation than those observed in the HF group. A concomitant reduction in the expression of Nrf2-dependent antioxidant genes was observed in the HF + NVD group. Furthermore, hepatic mitochondrial DNA content as well as hepatic SIRT1 mRNA level and activity, the NAD⁺/NADH ratio, and CPT1α mRNA expression were significantly decreased in the HF + NVD group. Conclusions: An inadequate vitamin D status was associated with greater hepatic lipid deposition, enhanced oxidative stress, and reduced hepatic SIRT1 activity, and lower expression of Nrf2-related antioxidant genes. These findings support that maintaining adequate vitamin D status might help preserve hepatic metabolic homeostasis during obesity. Full article

Background/Objectives: Pulmonary fibrosis is a progressive and fatal disease characterized by excessive extracellular matrix deposition and irreversible lung remodeling. Although modified mRNA (modRNA) therapeutics offer a promising strategy for regulating disease-driving pathways, effective pulmonary delivery remains challenging due to the inherent liver tropism of conventional lipid nanoparticles (LNPs). This study aimed to establish an optimized platform for lung-selective modRNA delivery and therapeutic screening for pulmonary fibrosis. Methods: A panel of charge-modified LNP formulations was evaluated in vivo for pulmonary tropism following systemic administration of luciferase (Luc) modRNA. Administration routes, biodistribution in healthy and bleomycin (BLM)-induced fibrotic lungs, and endogenous microRNA (miRNA)-mediated de-targeting strategies were assessed. Candidate antifibrotic modRNAs targeting the transforming growth factor-beta (TGF-β) signaling pathway were subsequently evaluated in normal human lung fibroblasts (NHLFs). Results: Among the formulations tested, 50% DOTAP MC3 LNPs demonstrated the most favorable balance of pulmonary transfection, physicochemical properties, and limited off-target expression. Intravenous (IV) administration achieved robust lung expression with a superior safety profile compared with intratracheal (IT) delivery. Importantly, pulmonary biodistribution was preserved in BLM-induced fibrotic lungs despite extensive tissue remodeling. Incorporation of miR-122 recognition sites further enhanced selectivity, resulting in 94.5% of total transgene expression being localized to the lungs while substantially reducing residual hepatic expression. In vitro screening identified dominant-negative TGF-β receptor II (DNTGFBR2) modRNA as a potent inhibitor of TGF-β-induced fibrotic activation, significantly suppressing α-SMA and CTGF expression. Conclusions: These findings establish a comprehensive platform for pulmonary modRNA therapeutic development by integrating lung-selective LNP engineering, optimal systemic delivery, miRNA-mediated de-targeting, and therapeutic payload screening. This strategy provides a foundation for the development of targeted RNA therapies for pulmonary fibrosis and other organ-specific diseases. Full article

Background/Objectives: Metabolic-dysfunction-associated steatotic liver disease (MASLD) and metabolic-dysfunction-associated steatohepatitis (MASH) arise in the setting of obesity, insulin resistance, type 2 diabetes, and metabolic syndrome. This review examines how mitochondrial dysfunction participates in the transition from lipid accumulation to hepatocyte injury, inflammation, and fibrosis, and how evidence from human, animal, and in vitro studies should be interpreted. Methods: We provide a narrative synthesis of mechanistic, translational, and clinical studies on hepatic mitochondrial metabolism, fatty acid oxidation, oxidative phosphorylation, redox stress, organelle crosstalk, mitophagy, mitochondrial biogenesis and proteostasis, mitochondrial danger signals, the gut-liver-mitochondria axis, and mitochondria-related therapeutic strategies. Results: In early metabolic overload, mitochondrial oxidation may increase as an adaptive response. With persistent substrate pressure, this adaptation can become inefficient, with impaired fatty acid disposal, less efficient oxidative phosphorylation, reactive oxygen species production, redox imbalance, defective mitochondrial quality control, altered mitochondrial biogenesis, mitochondrial unfolded protein response (UPRmt)-related proteostatic stress and mtDNA instability. Mitochondrial DNA and RNA released from damaged organelles may also activate cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING), inflammasome, and RNA-sensing pathways, linking hepatocyte stress to macrophage activation, stellate cell activation, extracellular matrix deposition, and fibrosis. Conclusions: The current evidence supports mitochondria as a stage-dependent amplifier of metabolic liver injury rather than a uniform initiating event. Clinically, the strongest evidence remains with upstream metabolic unloading and liver-directed metabolic therapy, whereas direct mitochondrial restoration and quality-control targeting remain promising but less mature. Full article

Fat deposition determines beef marbling grade and meat quality, but the underlying molecular mechanisms remain unclear. This study aimed to investigate the role of bovine PPARD in lipid deposition, especially its effect on the expression of fatty acid transport genes (CD36, FATP1, and FABP1) and the lipid droplet-associated gene (PLIN2) in liver tissues from cattle with different marbling grades. The mRNA abundance and protein levels in liver tissues from thirty-one Wagyu × Angus crossbred beef cattle (25–26 months old) with different marbling grades (according to GB/T 29392-2022, based on the marbling richness of the longissimus dorsi muscle at the 12th–13th rib interface) were analyzed by RT-qPCR and Western blot, respectively. Additionally, PPARD was knocked down and overexpressed in bovine mammary epithelial cells to validate its effects on lipid-metabolism-related genes. The results showed that the mRNA levels of CD36, FATP1, PPARD, RXRA, RXRB, and PLIN2 were significantly higher (p < 0.01) in livers tissues from the A3 and A4 groups (high marbling) than in those from the A1 and A2 groups (low to moderate marbling). Western blot analysis revealed significantly higher PPARD protein expression in the A3 and A4 groups (high marbling) than that in the A1 and A2 groups (low to moderate marbling) (p < 0.05). It should be noted that the sample size of Group A4 is only 2, and the results of this group should be considered as a preliminary trend that needs to be validated with larger sample sizes. Cellular experiments confirmed that PPARD knockdown significantly decreased mRNA expressions of FABP1, CD36, and PLIN2 (p < 0.01), while PPARD overexpression significantly increased their mRNA levels (p < 0.05). These results indicate a positive correlation between PPARD expression and the transcriptional levels of genes involved in fatty acid transport and lipid droplet storage, suggesting that PPARD may be associated with hepatic lipid metabolism and potentially contribute to marbling development. These findings suggest that the PPARD signaling pathway contributes to hepatic lipid deposition and may play a role in marbling formation in beef cattle. Full article

The replacement of fishmeal with plant-based ingredients in aquafeeds, while economically and environmentally advantageous, can impair lipid metabolism and liver function in fish due to the lack of specific bioactive compounds such as bile acids (BAs). BAs are amphipathic steroid molecules that facilitate lipid digestion and act as signaling hormones, yet their optimal inclusion levels in conventional, balanced diets for Nile tilapia (Oreochromis niloticus) remain undefined. This study evaluated the effects of dietary BA inclusion on growth performance, feed efficiency, body composition, and serum biochemical parameters of juvenile Nile tilapia (GIFT strain, initial weight 18.04 ± 3.67 g) and estimated the optimal inclusion level. Six isoproteic (320 g kg⁻¹) and isoenergetic (3300 kcal kg⁻¹) plant-based diets were formulated with increasing BAs levels (0, 50, 100, 200, 400, and 600 mg kg⁻¹) and fed to quadruplicate groups for 45 days. Only the Linear Response Plateau (LRP) model converged for weight gain data, estimating the optimal BA level at 479.70 mg kg⁻¹, with a plateau weight gain of 76.60 g. Inclusion of the 50–600 mg kg⁻¹ BAs significantly improved specific growth rate (up to 4.53%), crude protein retention efficiency (up to 81.11%), and whole-body crude protein content (up to 50.52%) compared to the control (p < 0.05). Fish fed 200 mg kg⁻¹ BAs exhibited the highest protein retention and lowest ether extract deposition, indicating a protein sparing effect. Serum lipase activity increased proportionally with BAs levels, while alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were reduced at 400 mg kg⁻¹ BAs, reflecting improved liver health. No mortality was recorded. In conclusion, dietary BAs inclusion enhances growth, protein utilization, and hepatic function in juvenile Nile tilapia fed plant-based diets. The recommended optimal level is 479.70 mg kg⁻¹ (dry matter basis), although significant benefits already occur from 50 mg kg⁻¹. These findings support the strategic use of BAs to improve the sustainability and efficiency of tilapia production. Full article

Oocyte quality determines fertilization success during the reproductive period of fish and is affected by a key intrinsic factor: the level of lipid deposition in the yolk. In this study, lipidomics was used to characterize lipid profiles of adipose tissue, liver, serum and ovary to clarify divergent hepatic lipid allocation to fat depots versus ovary in Sichuan taimen (Hucho bleekeri). The results showed that glycerophospholipids (GPs) constituted the most diverse lipid class across all four tissues, with phosphatidylcholine (PC) being the most abundant in each tissue. Relative to adipose tissue, liver, and serum, the ovary exhibited significant enrichment of PC and phosphatidylethanolamine (PE) and higher accumulation of docosahexaenoic acid (DHA)- and arachidonic acid (ARA)-containing GPs and triacylglycerols (TGs), as well as enrichment in TGs, diacylglycerols (DGs), and cardiolipin (CL), compared to adipose tissue. The expression levels of fads6, elovl2, elovl5, dgat1b, dgat2, pparα, nfyb, and fabp7 were higher in the liver, while lpcat1 was highly expressed specifically in the ovary. The results of this study demonstrate that long-chain polyunsaturated fatty acids (LC-PUFAs) exhibited selective enrichment in the ovary, which facilitates yolk lipid deposition and provides structural and energetic support for oocyte development and early embryonic development. From a lipidomic perspective, this study reveals the regulatory characteristics underlying ovarian yolk deposition in H. bleekeri, providing important evidence for understanding the mechanisms of egg quality formation as well as a theoretical basis for broodstock management, artificial propagation, and the improvement of egg and larval quality. Full article

Background: Oxidative stress and maladaptive cardiac remodeling are key contributors to heart failure progression. Xestospongia testudinaria, a marine sponge rich in bioactive compounds, possesses antioxidant and lipid-modulating properties. This study investigated the cardioprotective and antioxidant effects of Xestospongia testudinaria methanolic extract (Xesto) in an isoprenaline-induced rat model of heart failure. Methods: Thirty-five healthy male Wistar rats weighing 200–250 g were used in this study. Heart failure was induced in rats via subcutaneous administration of isoprenaline (10 mg/kg/day) for 14 days. Rats were subsequently treated with Xesto (15 mg/kg/day, oral gavage), digoxin (10 mg/kg/day), or saline for an additional 14 days. Hemodynamic parameters, serum NT-proBNP, oxidative stress biomarkers, biochemical indices, hematological parameters, and histopathological changes were evaluated. Molecular docking was performed to assess the interaction of Xesto constituents with Kelch-like ECH-associated protein 1 (KEAP1). Results: Isoprenaline administration significantly increased blood pressure, NT-proBNP, malondialdehyde, hepatic enzymes, and urea levels, while reducing superoxide dismutase and catalase activities. Xesto treatment significantly improved hemodynamic parameters, restored antioxidant enzyme activities, reduced lipid peroxidation, and normalized biochemical and hematological alterations. Histological analysis demonstrated reduced cardiomyocyte hypertrophy and collagen deposition in Xesto-treated rats. Docking analysis showed favorable binding of trans-phytol within the KEAP1 Kelch domain, suggesting possible modulation of antioxidant regulatory pathways. Conclusions: Xestospongia testudinaria exhibited significant cardioprotective and antioxidant effects in isoprenaline-induced heart failure, potentially through enhancement of endogenous antioxidant defenses and attenuation of pathological cardiac remodeling. These findings support its potential as a marine-derived therapeutic candidate for oxidative stress-associated cardiovascular disorders. Full article

Although praziquantel (PZQ) is the main antischistosomal drug currently in use, concerns remain regarding incomplete reversal of schistosomiasis-induced pathology and the emergence of drug resistance. This study evaluates the combined effect of PZQ with safranal, a bioactive saffron constituent, on Schistosoma mansoni-induced pathology in mice. Male CD1 Swiss albino mice were exposed to 60 S. mansoni cercariae and, at week 9 post-infection, were treated with PZQ (500 mg/kg orally for two consecutive days), safranal (50 mg/kg/day), or both, for three weeks. The animals were sacrificed at week 11 post-infection. Worm and egg burdens, liver histopathology, fibrotic markers, oxidative stress, and inflammatory cytokines were assessed. Combined PZQ + safranal therapy significantly reduced adult worm counts and hepatic and intestinal egg loads compared to PZQ alone. All treatments decreased liver index (hepatomegaly), with the combination treatment providing the best intervention. Histological analyses revealed significantly reduced granuloma size and hepatic necrosis post-treatment, particularly in the combination group. The levels of proinflammatory cytokines (TNF-α, IL-1β) and Th2 cytokines (IL-4, IL-5, IL-6, IL-10) were significantly lowered in treated mice, most notably with the combination treatment. Oxidative stress was also markedly attenuated, and infected mice exhibited elevated malondialdehyde and depleted antioxidant enzymes (SOD, CAT, GSH). Interestingly, PZQ and/or safranal restored antioxidant status and reduced lipid peroxidation, with the combination being most effective. Furthermore, collagen deposition and expression of hepatic fibrotic markers α-smooth muscle actin (α-SMA), TGF-β1, and matrix metalloproteinase-9 were most effectively suppressed by combined therapy. To conclude, safranal enhances PZQ’s antischistosomal efficacy and confers additive protection against Schistosoma-induced liver fibrosis. Full article

Introduction: Fish and humans share evolutionarily conserved pathways regulating lipid metabolism. However, the effects of pharmaceuticals on lipid homeostasis in fish remain poorly understood, particularly regarding mechanistic lipid dysregulation and its implications for fish physiology and environmental toxicology. While hypolipidemic drugs such as statins have been shown to modulate lipid metabolism in teleosts, other lipid-lowering agents, including cholesterol absorption inhibitors, remain largely unexplored. Additionally, synthetic hormones have been shown to interfere with lipid regulation, although their effects—particularly those of progestins—remain poorly characterized. Objective: This study aimed to explore the mechanistic lipid disruptions induced by potential hypo- and hyperlipidemic modulating pharmaceuticals in brown trout juveniles exposed to subchronic pharmacological conditions. Methodology: Juvenile brown trout were exposed via intramuscular injection every 72 h for 28 days and allocated into six experimental groups (n = 12 per group): control (C; 0.7% NaCl), solvent control (SC; 0.7% NaCl, 0.9% ethanol, 0.1% dimethyl sulfoxide), atorvastatin (ATV; 0.3 µg·g⁻¹), ezetimibe (EZB; 0.3 µg·g⁻¹), 17α-ethinylestradiol (EE2; 2 µg·g⁻¹), and levonorgestrel (LNG; 0.1 µg·g⁻¹). All concentrations represented pharmacological doses. On day 28, the fish were euthanized and sampled. Endpoints included biometric measurements, blood lipid profiling, serum biochemistry, and hepatic lipid accumulation. Results: ATV fish displayed greater body length, whereas EE2 increased liver weight and hepatosomatic index. EE2 reduced high-density lipoproteins and increased low-density lipoproteins, while atorvastatin reduced low-density lipoproteins. EE2 exposure also increased albumin levels and decreased glucose concentrations. Furthermore, EE2 significantly enhanced hepatic lipid deposition. Conclusions: The hyperlipidemic effects of EE2 were the most pronounced, whereas ATV produced the strongest hypolipidemic responses, consistent with its known effects in humans, and also influenced biometry. These findings provide a robust foundation for understanding how pharmaceuticals influence lipid metabolism and related physiological processes such as growth in fish, with relevance for both fish physiology research and environmental toxicology. 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

Aging-associated dyslipidemia and chronic low-grade inflammation contribute to atherosclerosis and cardiovascular risk. As a blend of long-chain aliphatic alcohols, policosanol from insect wax (PIW) has been documented to regulate lipid metabolism. However, the effects of PIW on atherosclerosis remain insufficiently characterized. In this study, ApoE^−/− mice fed a high-fat diet were concurrently administered PIW (75 and 150 mg/kg) for eight weeks. PIW was associated with weight gain reduction and improvement in lipid profile, particularly a decrease in triglycerides and total cholesterol. PIW also lowered circulating inflammatory biomarkers (IL-6, TNF-α, and C-reactive protein). Histopathological analyses revealed attenuated hepatic injury and reduced aortic lipid deposition and lesion features. In parallel, PIW reduced serum endothelin-1 and oxidized LDL levels and modulated aortic ET-1, MMP-9/TIMP-1 balance, and LOX-1/NF-κB-related protein signals. Notably, as PIW was administered concurrently with high-fat diet induction, these findings should be interpreted within a preventive intervention framework. Collectively, PIW help attenuate HFD-associated atherosclerotic features and hold promise as a functional food ingredient for cardiovascular health and healthy aging. Full article

Lipids play a central role in poultry nutrition by modulating energy utilization, nutrient digestibility, and metabolic processes related to lipid absorption and deposition. This review synthesizes current knowledge on the main dietary lipid sources used in poultry nutrition and their effects on performance, lipid metabolism, and egg yolk fatty acid composition. Conventional lipid sources, including vegetable oils and animal fats, differ in fatty acid profile, degree of saturation, and digestibility, which directly influence metabolic efficiency and productive responses. In addition, the strategic use of lipid sources enables the modulation of fatty acid profiles in poultry products, particularly through the enrichment of polyunsaturated fatty acids such as omega-3. These effects are associated with mechanisms involving lipid digestion, absorption, and hepatic lipoprotein synthesis, which regulate fatty acid deposition in tissues and egg yolks. However, responses to dietary lipids are influenced by factors such as inclusion level, oxidative stability, and lipid composition. Overall, dietary lipid manipulation represents an effective strategy to optimize production efficiency and enhance the nutritional quality of poultry-derived foods. Full article