Search Results (2,871)

Allomyrinasin is an antimicrobial peptide derived from the larvae of the edible insect Allomyrina dichotoma and has been reported to exert anti-inflammatory activity, although its role in metabolic regulation remains unclear. This study aimed to investigate the metabolic and hepatoprotective effects of allomyrinasin in a high-fat diet (HFD)–induced obese mouse model. Male C57BL/6J mice were fed an HFD for 6 weeks to induce body weight gain and hyperglycemia, followed by 10 weeks of oral administration of allomyrinasin (0.1 mg/kg/day) under continued HFD conditions, with metformin used as a positive control. Metabolic parameters related to glucose homeostasis, insulin sensitivity, lipid metabolism, hepatic injury, oxidative stress, inflammation, and fibrotic responses were evaluated. Allomyrinasin significantly attenuated HFD-associated body weight gain and improved glucose tolerance and insulin sensitivity. These effects were accompanied by favorable modulation of serum lipid profiles and suppression of hepatic lipogenic signaling, including reduced expression of key regulators of de novo lipogenesis. In parallel, allomyrinasin mitigated hepatic inflammatory, fibrotic, and oxidative stress-related alterations, as reflected by improvements in biochemical markers and molecular analyses. Collectively, these findings indicate that allomyrinasin contributes to the improvement of metabolic regulation and hepatic homeostasis in HFD-fed mice. Our results support allomyrinasin as a promising food-applicable bioactive peptide and potential functional ingredient for the prevention or management of obesity-related metabolic disorders. Full article

Plant-based symbiotic systems are often limited by poor storage stability and inconsistent biofunctional performance. This study evaluated the stability and functionality of a fermented blend based on sacha inchi (Plukenetia volubilis) oil press cake (SIC) and yacon (Smallanthus sonchifolius) flour (YF) as sources of protein and fructooligosaccharides (FOS), respectively, using two processing strategies: fermentation with Lactobacillus rhamnosus (T1) and combined enzymatic hydrolysis with Alcalase and fermentation with Lactobacillus plantarum (T2). Both treatments maintained viable cell counts (VCC) above probiotic thresholds (>10⁶ CFU mL⁻¹) during 28 days of storage at 4 °C, confirming their suitability as probiotic carriers. Notably, T2 significantly enhanced metabolic activity, as evidenced by higher organic acid production and increased soluble protein content due to Alcalase-mediated hydrolysis, which promoted the generation of bioactive peptides associated with improved antioxidant and antihypertensive activities. Biofunctional properties, including total phenolic content, antioxidant capacity (AC), and angiotensin-converting enzyme (ACE) inhibitory activity, remained stable throughout storage, while FOS degradation was minimal, confirming preservation of prebiotic functionality. LC–MS/MS Q-TOF analysis revealed a complex phenolic profile that was differentially modulated by lactic acid fermentation, with L. plantarum (T2) promoting extensive phenolic biotransformation and increased metabolite diversity, whereas L. rhamnosus (T1) largely preserved the original phenolic profile. These findings demonstrate that the synergistic interaction between enzymatic hydrolysis and L. plantarum fermentation promoted peptide release, intensified microbial metabolism, and enhanced phenolic biotransformation, thereby contributing to the superior functional properties observed in T2, while maintaining stable biofunctional characteristics throughout refrigerated storage in both treatments. 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

Cutaneous infections and chronic inflammatory wounds remain difficult to treat because antimicrobial resistance, polymicrobial biofilms, excessive protease activity, oxidative stress, and impaired barrier repair collectively reduce the effectiveness of conventional topical therapies. Plant-derived antimicrobial peptides (AMPs) and peptide-associated bioactives offer antimicrobial, antibiofilm, immunomodulatory, and tissue reparative potential; however, their clinical translation is limited by proteolytic instability, poor stratum corneum penetration, short cutaneous residence time, formulation variability, cytotoxicity risks and limited human evidence. The key research gap is the lack of an integrated translational framework linking plant-derived peptide bioactivity with polymer engineering, advanced delivery systems, skin microenvironment biology, manufacturability, and regulatory feasibility. This review aims to critically evaluate the design principles, therapeutic mechanisms, delivery platforms, and translational barriers of plant-based peptide–polymer therapeutics for cutaneous infection and inflammation. We summarize major classes of plant-derived antimicrobial peptides, including defensins, cyclotides, thionins, hevein-like peptides, snakins, lipid transfer proteins, and knottin-type scaffolds, and examine engineering strategies such as self-assembly, aromatic N-capping, PEGylation, lipidation, dendritic architectures, and stimuli-responsive conjugation. We further discuss topical matrices, nanocarriers, liposomes, electrospun fibers, and surface-tethered biomaterials as delivery platforms for improving peptide stability, local retention, and controlled release. Finally, we identify key translational bottlenecks, including selectivity, toxicity, scalability, batch reproducibility, regulatory classification, and insufficient clinical validation. Mechanism-driven peptide optimization, quality-by-design manufacturing, standardized preclinical models, and controlled clinical trials will be essential for advancing these systems toward safe and effective dermatological therapies. Full article

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

Cancer, a longstanding global challenge, remains a leading cause of death, prompting an urgent search for effective treatments. Conventional therapies, while prevalent, often cause adverse effects due to their lack of specificity. This review explores an innovative approach, focusing on animal toxins as a rich source of bioactive compounds which have demonstrated efficacy against cancer cells. Peptides from various species, including scorpions, snakes, bees, spiders, and frogs, show promising antiproliferative and cytotoxic effects. Emphasizing the most prevalent types of cancer, this review outlines the discovery and development stages of potential anticancer drugs derived from toxin peptides. The comprehensive overview includes in vitro and in vivo assessments of their anticancer activity and toxicity. This pioneering exploration extends to different tumors, offering valuable insights into mechanisms of action and potential therapeutic applications. The findings highlight a paradigm shift in cancer research, showcasing the potential of toxin-derived compounds for developing targeted and efficient cancer therapies with reduced side effects. Full article

Pathogenesis-related 1 (PR1) proteins are important components of plant defense and stress responses and also serve as precursors of CAP-derived peptides (CAPE), a class of small bioactive peptides involved in immune and stress signaling. Despite their potential biological significance, CAPE-producing PR1 genes have not been systematically characterized in tobacco (Nicotiana tabacum). In this study, a genome-wide analysis identified 17 CAPE-producing PR1 genes, designated NtCAPE1 to NtCAPE17, in the tobacco genome. These genes encode proteins containing conserved CAP domains and N-terminal signal peptides, with predicted hydrophilic properties and mainly vacuolar localization, indicating conserved structural features within the family. Phylogenetic analysis, gene structure organization, conserved motif profiling, chromosomal distribution, and synteny analyses revealed both evolutionary conservation and duplication-driven diversification of the NtCAPE family. Promoter cis-element analysis showed enrichment of regulatory elements associated with phytohormone signaling, development, and stress responses. Public transcriptomic datasets revealed dynamic and gene-specific expression patterns under water-deficit and salinity stress, and qRT-PCR analysis further confirmed the stress-responsive expression of selected NtCAPE genes. Functional assays using synthetic mature peptides showed that NtCAPE9 and NtCAPE17 alleviated salinity stress- and osmotic stress-induced leaf yellowing, improved chlorophyll retention, suppressed senescence-associated responses, reduced H₂O₂ accumulation and POD activity, modulated stress-responsive gene expression, and promoted seed germination under salinity and osmotic stress, respectively. These results provide a comprehensive characterization of CAPE-producing PR1 genes in tobacco and identify NtCAPE9 and NtCAPE17 as candidate stress-associated peptides with exogenous activity under salinity and osmotic stress conditions. Full article

Coconut kernel fiber (CKF) is a by-product of coconut oil processing; it is rich in protein and serves as a potential source of bioactive peptides. In this study, from the enzymatic hydrolysis products of CKF (CKFH), a low-molecular-weight CKFH component (LW-CKFH, 1–3 kDa), exhibiting 74.49% α-glucosidase inhibition and restoring glucose metabolism in IR-HepG2 cells to 71.37% of normal levels. In a type 2 diabetes (T2DM) mouse model, LW-CKFH alleviated insulin resistance and enhanced insulin sensitivity by repairing liver damage, thereby improving glucose and lipid metabolism and reducing inflammation; its effects on improving insulin resistance and sensitivity reached 75.43% and 75.47% of the efficacy of metformin, respectively. Molecular docking analysis identified FDLPAR, LPFPRPAGPR, and ANVFNPR as key active peptides responsible for inhibiting α-glucosidase activity. Furthermore, LW-CKFH exhibited good gastrointestinal digestibility and processing stability, while significantly reducing the glucose release rate from bread (>50%), indicating its suitability for the development of hypoglycemic or low-GI functional foods. LW-CKFH was particularly suitable as a functional ingredient for fruits, vegetables, grains, and dairy products to develop low-GI or hypoglycemic foods. This study provides new insights into the high-value utilization of the coconut processing by-product CKF. Full article

Inflammatory bowel disease (IBD; Crohn’s disease and ulcerative colitis) arises from convergent dysfunction of the epithelial barrier, mucosal immunity, and gut microbiome on a background of genetic susceptibility and environmental exposures. Diet is among the most modifiable of these exposures, yet much of the diet–microbiome research in IBD remains descriptive and poorly aligned with the molecular pathways linking food to mucosal effects. This comprehensive review reframes the field around functional dysbiosis, in which altered microbial metabolic capacity (rather than taxonomic shifts alone) drives disease-relevant biology. We trace how dietary substrates and additives are converted by gut microbes into bioactive metabolites (short-chain fatty acids, secondary bile acids, tryptophan-derived indoles, sulfur compounds, and polyphenol-derived molecules) and map these to host receptors and signaling pathways governing barrier function, mucus and antimicrobial peptide production, and Treg/Th17 balance. Defined dietary therapies (exclusive enteral nutrition, the Crohn’s disease exclusion diet plus partial enteral nutrition, and Mediterranean-style patterns) are reinterpreted as interventions that reshape microbial metabolic output, and candidate biomarkers for microbiome-informed precision nutrition are evaluated. Microbiota-derived metabolites provide the molecular interface between diet and mucosal immunity in IBD; personalized dietary algorithms remain a research goal, not a validated clinical tool, and diet is best framed as adjunctive to pharmacotherapy and dietitian care. Full article

Food-derived bioactive peptides have become a research hotspot in diabetes nutritional intervention due to their high safety, wide availability, and multi-target activities. This review addresses this by proposing a systems biology integration framework that defines these peptides as pleiotropic regulators of the gut microbiota-immune inflammation-metabolic signaling network, offering a novel systems-level perspective beyond previous reviews focused on single enzymes or pathways. The framework consists of three synergistic tiers. Tier 1 inhibits α-amylase, α-glucosidase or dipeptidyl peptidase-IV (DPP-IV) to control postprandial blood glucose. Tier 2 corrects insulin resistance by modulating phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), activating nuclear factor erythroid 2-related factor 2 (Nrf2), and suppressing nuclear factor kappa-B (NF-κB). Tier 3 uses the gut as a hub to remotely coordinate metabolism via the gut–liver and gut–pancreas axes. The review also systematically summarizes the major sources and preparation methods of food-derived antidiabetic peptides, analyzes their advantages including multi-target network regulation, safety, and sustainability, as well as challenges such as oral bioavailability, insufficient clinical evidence, processing stability, and regulatory hurdles. Finally, it outlines future directions focusing on three actionable priorities: AI-assisted design, oral delivery systems, and high-quality clinical studies. This framework offers a new perspective for applying food-derived peptides in precision nutrition intervention for diabetes. Full article

To address the poor solubility, instability, and low oral bioavailability of quercetin (Q), Q-loaded nanoparticles (Q@DDZ) were fabricated using deamidated zein peptide (DDZ) via a pH-driven method. As a food-grade hydrophilic colloid, DDZ effectively improves the colloidal stability of the delivery system. Deamidation increased hydrophilic amino acids and surface negative charge. DDZ bound Q via static quenching with a higher binding constant (K_a = 2.25 × 10³ L/mol) and more binding sites (n = 1.7561) than zein, along with stronger hydrogen bonding and hydrophobic interactions. Q@DDZ exhibited higher encapsulation efficiency (45.36–87.32%) and loading capacity (1.82–12.27%) than Q@zein, with a smaller particle size and better dispersibility. At 50.0 μg/mL Q, Q@DDZ showed 41.06% (DPPH) and 46.62% (ABTS) higher scavenging rates than free Q. It displayed excellent stability under acidic, high ionic strength, and thermal conditions (80 °C, 180 min). In simulated digestion, Q@DDZ delayed Q release in the oral and gastric phases and prolonged intestinal release, which indicated potentially improved bioavailability. This study provides mechanistic insights into deamidation-modified plant protein delivery systems for hydrophobic bioactives, offering new perspectives for the development of functional biopolymer gel materials. Full article

Obesity and its metabolic complications represent a major global health challenge, and food-derived bioactive peptides are emerging as promising dietary interventions. In this study, two hemp seed protein-derived tetrapeptides with pancreatic lipase (PL) and cholesterol esterase (CE) inhibitory activity, APAM and RLPA, were co-administered with a high-fat diet (HFD) to male C57BL/6J mice at 25 and 100 mg/kg body weight for 10 weeks. Both peptides dose-dependently alleviated HFD-induced body weight gain, visceral fat accumulation, hepatic steatosis, dyslipidemia, hyperglycemia, and systemic inflammation. Mechanistically, both peptides inhibited intestinal PL and CE activities and enhanced fecal lipid excretion, supporting direct suppression of intestinal fat digestion. 16S rRNA gene sequencing revealed partial restoration of HFD-disrupted gut microbiota, with APAM preferentially enriching Bifidobacterium and Roseburia, while RLPA promoted Akkermansia and Lactobacillus, accompanied by differential improvements in fecal short-chain fatty acid (SCFA) profiles. Hepatic transcriptomics identified the PPAR signaling pathway as a shared regulatory hub, and multi-omics integration revealed significant correlations linking gut microbiota, SCFA production, hepatic gene expression, and metabolic phenotypes. These findings suggest a dual-pathway anti-obesity mechanism integrating intestinal lipid digestion inhibition with gut–liver axis modulation, and highlight hemp seed protein-derived peptides as potential functional food ingredients for obesity prevention. Full article

Extracellular vesicles (EVs) have attracted considerable attention as natural nanocarriers for immune modulation owing to their intrinsic biocompatibility, nanoscale size, and capacity to transport diverse bioactive cargos. In inflammatory diseases, EV-based therapeutics provide unique opportunities to regulate dysregulated immune responses; however, their clinical translation remains constrained by limited cell-specific targeting efficiency and uncontrolled biodistribution. Achieving precise and selective delivery to immune cells and other inflammation-associated cellular components within diseased tissues is therefore critical for maximizing therapeutic efficacy while minimizing off-target effects. This review comprehensively summarizes recent advances in cell-specific EV-targeting strategies for immune modulation in inflammatory diseases, with a particular focus on active targeting approaches enabled by EV surface engineering. A range of targeting ligands, including antibodies, peptides, aptamers, glycans, and membrane proteins, is discussed in the context of enhancing selective interactions between EVs and specific immune cell subsets. Special emphasis is placed on cell-directed targeting strategies toward diverse immune cell populations, including macrophages and T cells, highlighting how rational control of EV–cell interactions can be utilized to reprogram immune phenotypes, suppress pathological inflammation, and restore immune homeostasis. Accordingly, this review integrates recent progress in cell-specific EV targeting into a coherent conceptual framework, which may assist researchers in the rational design of EV-based immunomodulatory therapeutics. Full article

The gut microbiota (GM) has become a key mediator of host health, with dietary manipulations promising ways of modulating the microbiome. This review focuses on the role of dairy bioactive (DB) compounds as precision modulators of intestinal microecology, including the whey proteins (WPs), including lactoferrin (LF), α-lactalbumin (LA), β-lactoglobulin, lysozyme (LZ), lactoperoxidase, glycomacropeptide (GMP), milk oligosaccharides (MOs), and bioactive peptides (BPs). This review compiles the existing evidence illustrating their dual-action mechanism through direct prebiotic activity and the promotion of beneficial taxa (Bifidobacterium, Lactobacillus, Faecalibacterium), along with selective antimicrobial activity and pathogen suppression. These compounds improve intestinal barrier integrity through tight junction (TJ) protein regulation, regulating short-chain fatty acid production, and modulating immune signaling pathways. Clinical evidence shows significant benefits in metabolism and inflammation among various populations. However, individual responses vary according to host factors such as enterotypes, FUT2 genotype, and baseline microbiota composition, suggesting the need for personalized intervention strategies. This review addresses critical knowledge gaps in dose–response relationships, long-term efficacy, and mechanistic pathways and suggests future directions for precision nutrition. By modifying molecular mechanisms in clinical applications, we have identified DB compounds as promising candidates for targeted modulation of the microbiota to optimize health and disease management. The review also brings together molecular mechanistic and clinically implementable, personalized dietary strategies, which have not been fully captured by previous reviews. It pinpoints gaps in knowledge related to dose–response characterization, long-term trial design, and multi-omics stratification that collectively define a new precision nutrition framework. In this approach, dairy-based intervention is planned for each person based on their microbial, genetic, and metabolic characteristics. Full article

Mucormycosis is a devastating invasive fungal infection primarily caused by Mucor and Rhizopus species, presenting significant clinical challenges due to limited therapeutic options and emerging drug resistance in opportunistic yeasts such as Candida albicans. This study explores foliar endophytic fungi from Thai medicinal plants as potential reservoirs for novel bioactive metabolites targeting both fungal growth and virulence factors. We report the first isolation of Fusarium proliferatum as an endophyte from Lantana camara L. foliage (voucher number 01562), with its identity confirmed through morphological characterization and sequencing of the fungal ITS4/ITS5 regions. Antifungal susceptibility testing showed potent activity against a panel of environmental Mucorales, with minimum inhibitory concentrations (MICs) ranging from 0.3 to 1 mg/L. In dual-culture assays, F. proliferatum demonstrated significant mycelial inhibition rates of 93.30% to 93.67% against Mucor spp. and 88.67% to 93.67% against Rhizopus spp. Furthermore, the crude extract exhibited a potent anti-virulence effect by suppressing the C. albicans yeast-to-hyphal transition, achieving up to 68% germination inhibition in resistant strains. Liquid chromatography–mass spectrometry (LC-MS) analysis identified 51 secondary metabolites, including the cyclic peptide beauvericin and various polyketides and indole derivatives. These findings suggest that F. proliferatum utilizes metabolic mimicry and adaptive synergy with its host plant to produce a diverse chemical arsenal. This study positions foliar endophytes of L. camara as promising candidates for the development of dual-action therapeutics to combat invasive and resistant mycoses. Full article