Search Results (12,215)

Lipids play important roles in maintaining pulmonary structure, performing physiological functions and controlling the immune status of the lung. There is increasing evidence that lipid metabolism and immune activity are closely linked and that dysfunction in lipid metabolism contributes to the development and progression of chronic respiratory diseases such as COPD and asthma. These diseases are characterized by metabolic and immune dysregulation, with lipid mediators playing a key role in both the development and resolution of inflammation. In this regard, lipid metabolic pathways are attracting increasing attention as promising targets for biomarker detection and therapeutic intervention. Full article

Background: Metabolic dysfunction-associated fatty liver disease (MASLD) is closely associated with immune dysregulation and macrophage-driven inflammation. The activation of PPARG plays a critical role in modulating macrophage polarization and lipid metabolism, suggesting its potential as a therapeutic target for MASLD. Methods: We used UPLC-Q/TOF-MS and network pharmacology to investigate the key components and targets of Swertia davidi Franch, focusing on Swertianin. In vitro experiments on macrophages were conducted to assess the modulation of M1 polarization, and a mouse model of MASLD was utilized to explore the therapeutic effects of Swertianin. Results: Swertianin activated PPARG, leading to significant inhibition of M1 macrophage polarization, a reduction in lipid accumulation, and decreased inflammatory marker levels both in vitro and in vivo. The treatment significantly improved liver pathology in mice, indicating its therapeutic potential for MASLD. Conclusion: Swertianin’s activation of PPARG provides a novel mechanism for treating MASLD, targeting both macrophage polarization and inflammation. Full article

This study compared the metabolic consequences of fecal microbiota transplantation (FMT) from donor mice that had been either administered pulsed electromagnetic field (PEMF) therapy or exercised to recipient mice fed a high-fat diet (HFD). Eight weeks of PEMF treatment (10 min/week) enhanced PGC-1α-associated mitochondrial and metabolic gene expression in white and brown adipose to a greater degree than eight weeks of exercise (30–40 min/week). FMT from PEMF-treated donor mice recapitulated these adipogenic adaptations in HFD-fed recipient mice more faithfully than FMT from exercised donors. Direct PEMF treatment altered hepatic phospholipid composition, reducing long-chain ceramides (C16:0) and increasing very long-chain ceramides (C24:0), which could be transferred to PEMF-FMT recipient mice. FMT from PEMF-treated mice was also more effective at recovering glucose tolerance than FMT from exercised mice. PEMF treatment also enhanced bone density in both donor and HFD recipient mice. The gut Firmicutes/Bacteroidetes (F/B) ratio was lowest in both the directly PEMF-exposed and PEMF-FMT recipient mouse groups, consistent with a leaner phenotype. PEMF treatment, either directly applied or via FMT, enhanced adipose thermogenesis, ceramide levels, bone density, hepatic lipids, F/B ratio, and inflammatory blood biomarkers more than exercise. PEMF therapy may represent a non-invasive and non-strenuous method to ameliorate metabolic disorders. Full article

Microbial contamination is the leading cause of foodborne diseases and spoilage in food and personal care products. Previous studies by our group have demonstrated that vine tea extract (VTE) and dihydromyricetin (DMY) inhibit the growth of Escherichia coli. In this study, we further explored the inhibitory mechanisms of VTE and DMY against E. coli through a label-free proteomics approach. The proteomic analysis detected 130 and 81 differentially expressed proteins (DEPs) in E.coli following VTE and DMY treatment, respectively. The analysis indicated that VTE and DMY inhibit bacterial growth through multiple-target mechanisms. Specifically, they inhibit E. coli growth by disrupting the cationic antimicrobial peptide resistance pathway, amino acid biosynthesis and metabolism, and nucleotide metabolism. Additionally, VTE disrupts various secondary metabolic pathways, while DMY interferes with E. coli ribosome assembly and function, and disrupts cell membrane lipid homeostasis by interfering with fatty acid metabolism. RT-qPCR validation confirmed transcriptional alterations in genes encoding key target proteins. Molecular docking results indicated that DMY may affect bacterial protein synthesis, cationic antimicrobial peptide resistance, and transcriptional regulation by binding to target proteins such as RplB, RplV, LpxA, and YafC. In conclusion, this study systematically deciphered the multi-target inhibitory mechanisms of VTE and DMY against E. coli, providing a theoretical basis for developing plant-derived antimicrobial agents. Full article

Zinc-alpha2-glycoprotein (ZAG) is a soluble glycoprotein primarily produced in adipocytes and the liver, with key roles in lipid metabolism, including lipolysis and the browning of adipose tissue. Despite extensive studies on its role in rodents, the relationship between ZAG and insulin in humans remains unclear. Given the emerging interest in ZAG’s involvement in metabolic diseases such as metabolic-dysfunction-associated steatotic liver disease, this study aimed to investigate the acute effects of insulin on ZAG levels both in vivo and in vitro. We recruited 24 healthy, individuals who were non-obese and assessed the impact of oral glucose overload, a standardized liquid nutritional supplement, and intravenous glucagon on circulating ZAG levels. In parallel, we explored the effects of insulin on ZAG production in cultured HepG2 cells. Our findings revealed a consistent acute reduction in serum ZAG levels following all in vivo tests, coinciding with increased insulin levels. In vitro, insulin rapidly downregulated ZAG protein and mRNA levels in HepG2 cells, with significant reductions observed within 15 min, followed by partial recovery after 2 h. These results suggest a potential acute inhibitory effect of insulin on ZAG production, supporting its role in promoting energy storage by suppressing lipolysis postprandially. This study provides new insights into the complex interplay between insulin and ZAG in regulating energy balance and highlights the potential of ZAG as a therapeutic target in metabolic diseases. Full article

Essential fatty acids are extremely important nutrients in the diet of fish, and the balance between arachidonic acid (ARA) and eicosapentaenoic acid (EPA) is crucial for the healthy growth of fish. Six isonitrogenous and isolipidic basal diets were given to 540 juvenile fat greenling (Hexagrammos otakii) (31.4 ± 1.5 g) for 8 weeks to investigate the effects of dietary ARA/EPA ratio on growth performance, antioxidant capacity and lipid metabolism-related genes of juvenile H. otakii. The control group (A) had 7% fish oil added as the main fat source, while the experimental groups had 4% fish oil as the basic fat source, with varying proportions of ARA and EPA concentrates added to formulate five diets with varying ARA/EPA ratios (B 2.66; C 1.34; D 1.01; E 0.47; F 0.19). The experimental results revealed that adding ARA and EPA to the diet increased the percent weight gain (PWG) and feed conversion ratio (FCR) of juvenile H. otakii, and the PWG and FCR were greatest under Group E dietary conditions. The specific activities (U/mg protein) of superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (T-AOC) in the liver, as well as serum SOD and CAT were significantly higher in Groups D and E than those in other groups (p < 0.05). Malondialdehyde (MDA, nmol/g protein) content in the liver and serum was significantly lower in Group E than that in other groups (p < 0.05). Moreover, groups D and E exhibited significant increases in the specific activities (U/mg protein) of intestinal trypsin, lipase, and amylase, as well as in the intestinal villus length (p < 0.05). The incorporation of ARA and EPA into the feed reduced the expression levels of fat synthesis genes such as fas, scd1, accα, and srebp1, as well as the expression of lipolysis genes atgl and hsl. However, it also increased the expression of the lipolytic genes cpt1 and ppara. The ARA/EPA ratios in the dietary were 0.47 and 1.01, respectively, which are appropriate for enhancing growth efficiency, antioxidant enzyme activity, intestinal digestive enzyme activity and lipid metabolism regulation. Full article

The gut–adipose tissue axis plays a crucial role in metabolic health. It is a two-way communication pathway between the gastrointestinal tract and adipose tissue. This axis influences physiological processes vital for maintaining metabolic health, including energy homeostasis, lipid metabolism, and inflammation. Emerging research suggests that the gut microbiota, composed of trillions of microorganisms residing in the intestines, significantly impacts this axis by modulating host metabolism. An imbalance in the gut microbiota (dysbiosis) has been linked to obesity, insulin resistance, and other metabolic disorders. Innovative therapeutic strategies and dietary interventions aimed at modulating the gut–adipose tissue axis have shown encouraging results in improving metabolic health. A deeper critical understanding of the gut–adipose tissue axis is, therefore, essential in understanding the pathophysiology of metabolic disorders so that targeted interventions can be developed to prevent and treat these metabolic disorders. This article highlights the need for integrative approaches that consider both gastrointestinal and adipose functions in metabolic health management. Full article

Breast cancer metastasis remains the primary driver of patient mortality, involving dynamic interactions between tumor cells and distant organ microenvironments. In recent years, tumor cell-derived extracellular vesicles (EVs) have emerged as critical information carriers, playing central roles in breast cancer metastasis by mediating organ-specific pre-metastatic niche formation, immune modulation, and tumor cell adaptive evolution. Studies have demonstrated that EVs drive the metastatic cascade through the delivery of bioactive components, including nucleic acids (e.g., miRNAs, circRNAs), proteins (e.g., integrins, metabolic enzymes), and lipids, which collectively regulate osteoclast activation, immune cell polarization, vascular permeability alterations, and extracellular matrix (ECM) remodeling in target organs such as bone, the lungs, and the liver. Molecular heterogeneity in EVs derived from different breast cancer subtypes strongly correlates with organotropism, providing potential biomarkers for metastasis prediction. Leveraging the organotrophic mechanisms of EVs and their dual regulatory roles in metastasis (pro-metastatic and anti-metastatic), strategies targeting EV biogenesis, cargo loading, or delivery exhibits translational potential in diagnostics and therapeutics. In this review, we summarize recent advances in understanding the role of breast cancer-derived exosomes in mediating metastatic organotropism and discuss the potential clinical applications of targeting exosomes as novel diagnostic and therapeutic strategies for breast cancer. Full article

Algae-based supplements are gaining attention for their potential metabolic, antioxidant, and anti-inflammatory properties in sports nutrition. Methods: A 30-day pilot randomized controlled trial was conducted in 70 healthy male athletes (mean age 25.4 ± 4.9 years) from competitive soccer and handball teams. Participants were randomly assigned to a supplementation group (6 g/day of Ulva-derived algae powder) or a control group. Both groups followed identical training routines and adhered to standardized nutritional recommendations, including macronutrient distribution and permitted supplements (e.g., isotonic drinks, protein shakes). Biochemical markers analyzed at baseline and post-intervention included HbA1c, lipid profile, malondialdehyde (MDA), catalase, myeloperoxidase (MPO), erythrocyte sedimentation rate (ESR), and cortisol. Genetic polymorphisms related to metabolic traits were also assessed. Results: Significant group × time interactions (p < 0.001) were observed for HbA1c, LDL, triglycerides, MDA, MPO, ESR, and cortisol, all of which improved in the algae-supplemented group. Correlation analysis revealed associations between HbA1c and LDL/TG as well as between cortisol and MPO. No significant genetic modulation of responses was detected, although a trend was noted for cortisol variation and insulin resistance risk. Conclusions: Algae-based supplementation led to favorable metabolic, oxidative, and inflammatory changes. These findings suggest its potential utility as a nutritional strategy to support recovery in athletes during periods of high training load or competition. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease globally, and current estimates indicate an increase in incidence and prevalence in the general population. The design of the prospective study was to evaluate the response of patients with MASLD to an original formula consisting of silymarin, vitamin E, and essential phospholipids. In total, 200 patients were initially enrolled in the study and a total of 190 who participated in all four visits were included in our analysis. During the visits, liver function tests, lipid profiles, blood glucose level, fibrosis, and steatosis values and grades were assessed. From baseline, visit 0, to month 6th, visit III, a statistically significant difference (p-value < 0.0001) was observed in the reduction in ALT, AST, GGT, ALP, TG, total cholesterol, and blood glucose levels. There was a significant decrease in the fibrosis value from the first visit to the last visit (p = 0.002). Even though administered separately, silymarin, essential phospholipids, and vitamin E have established their efficacy in MASLD, this study demonstrates that their combination produces an indubitable effect on liver steatosis, even in a short cure of 6 months, and it can be proposed due to it having no adverse effects on patients with MASLD. Full article

The gut-liver-adipose axis plays a pivotal role in metabolic regulation, and its dysregulation contributes to obesity and metabolic syndrome. Probiotics and polycosanol have shown potential in modulating gut barrier integrity, lipid metabolism, and inflammation. This study aimed to evaluate their combined effects using an in vitro model of the gut-liver-adipose axis. Transwell^® system was used to recreate the interaction between intestinal (CaCo-2), hepatic (HepG2), and adipose (3T3-L1) cells. Cells were treated with Bifidobacterium bifidum GM-25, Bifidobacterium infantis GM-21, Lacticaseibacillus rhamnosus GM-28, and polycosanols. The effects were assessed by analyzing intestinal barrier integrity (TEER, tight junction proteins), hepatic and adipose lipid accumulation (Oil Red O staining), oxidative stress (ROS production, lipid peroxidation), inflammation (TNF-α) and lipid metabolism (CD36, PPARγ, AMPK and SREBP-1 levels). Probiotics and polycosanols improved intestinal integrity, increased butyrate production, and reduced ROS levels. Hepatic lipid accumulation was significantly decreased, with enhanced PPARγ and AMPK activation. In adipocytes, probiotic-polycosanols treatment suppressed SREBP-1 expression, enhanced lipid oxidation, and promoted UCP1 and PGC-1α expression, suggesting activation of thermogenic pathways. These findings underline a possible biological relevance of probiotics and polycosanols in modulating metabolic pathways, improving gut barrier integrity, and reducing inflammation, supporting their role as functional ingredients for metabolic health. Full article

Maternal metabolic dysfunction adversely influences embryonic muscle oxidative capacity and mitochondrial biogenesis, increasing the child’s long-term risks of developing obesity and metabolic syndrome in later life. This pilot study explored the mechanistic basis of embryonic muscle metabolic programming, employing non-invasive magnetic field exposures. Brief (10 min) exposure to low-energy (1.5 milliTesla at 50 Hertz) pulsing electromagnetic fields (PEMFs) has been shown in mammals to promote oxidative muscle development, associated with enhanced muscular mitochondriogenesis, augmented lipid metabolism, and attenuated inflammatory status. In this study, quail eggs were used as a model system to investigate the potential of analogous PEMF therapy to modulate embryonic muscle oxidative capacity independently of maternal influence. Quail eggs were administered five 10-min PEMF exposures to either upward-directed or downward-directed magnetic fields over 13 days. Embryos receiving magnetic treatment exhibited increased embryo weight, size, and survival compared to non-exposed controls. Upward exposure was associated with larger embryos, redder breast musculature, and upregulated levels of PPAR-α and PGC-1α, transcriptional regulators promoting oxidative muscle development, mitochondriogenesis, and angiogenesis, whereas downward exposure augmented collagen levels and reduced angiogenesis. Exposure to upward PEMFs may hence serve as a method to promote embryonic growth and oxidative muscle development and improve embryonic mortality. Full article

Crop productivity is severely constrained by abiotic and biotic stresses, necessitating innovative strategies to enhance stress resilience. Glycerol-3-phosphate (G3P) is a central metabolite in carbohydrate and lipid metabolism, playing crucial roles in stress responses. In this study, we engineered a novel glycerol-3-phosphate dehydrogenase (GPDH) gene, designated OEGD, by fusing the N-terminal NAD-binding domain of rice OsGPDH1 with the feedback-resistant C-terminal catalytic domain of Escherichia coli gpsA. Overexpression of OEGD in rice enhanced tolerance to drought, phosphorus deficiency, high temperature, and cadmium (Cd²⁺) stresses, while also improving plant growth and yield under drought stress at the adult stage. Notably, the accumulation of glycerol-3-phosphate (G3P) and activities of antioxidant enzymes (SOD, POD, CAT) were significantly elevated in the transgenic plants following osmotic stimuli, and fatty acid profiles were altered, favoring stress adaptation. Transcriptomic analyses revealed that OEGD modulates cell wall biogenesis, reactive oxygen species (ROS) scavenging, and lipid metabolism pathways, with minimal disruption to core G3P metabolic genes. These findings highlight the potential of OEGD as a valuable genetic resource for improving stress resistance in rice. Full article