搜索结果：Nutrition and metabolic insights

Metabolic dysfunction is a major driver of global chronic disease, yet current dietary guidance remains only loosely connected to the biological pathways that underlie these conditions. Historically, nutrition research emphasized individual nutrients or caloric content, overlooking the integrated metabolic effects of whole dietary patterns. Extensive research has linked dietary factors with chronic inflammation, insulin hypersecretion, and insulin resistance, with more recent studies synthesizing these associations into metabolically grounded dietary pattern indices, compared with the conventional nutrient- or calorie-focused approaches. Metabolic dietary patterns, empirically derived food-based indices that predict long-term metabolic biomarkers such as C-peptide and inflammatory cytokines, introduce mechanistic specificity into dietary assessment. This perspective reviews the development and evidence base of these patterns, compares them with conventional dietary pattern approaches, and synthesizes their nutritional characteristics and disease predictive capacity. Although many healthy dietary patterns are associated with improved chronic disease outcomes, metabolic dietary patterns show more consistent and robust associations, suggesting that targeting insulin resistance, a central hub connecting hyperinsulinemia, inflammation, and chronic disease, may better capture metabolically meaningful dietary variation. Because existing evidence is largely observational, we propose a structured translational framework for evaluating metabolic dietary patterns in clinical and community settings. Key tenets include preserving metabolic integrity; clarifying food and beverage intake targets; addressing items with uncertain or counterintuitive metabolic properties; accounting for food combinations and preparation methods; integrating food processing level; and ensuring cultural adaptability. This framework supports the translation of metabolic insights into actionable dietary guidance for precision prevention, clinical care, and public health.

Precision nutrition has emerged as a promising strategy for the prevention of type 2 diabetes mellitus (T2DM) by targeting molecular pathways underlying insulin resistance and impaired glucose metabolism. Accumulating evidence indicates that dietary patterns, caloric intake, and specific nutrients can modulate gene expression and epigenetic mechanisms involved in insulin signaling, inflammation, and energy homeostasis. This narrative review synthesizes recent human and experimental studies (2025-2026) examining how dietary components influence transcriptional and epigenetic regulation of insulin signaling and glucose metabolism in the context of T2DM prevention. A total of 29 peer-reviewed studies were included, encompassing dietary patterns, macronutrient manipulation, micronutrient and bioactive supplementation, and gene-diet interactions. Very-low-calorie diets consistently induced coordinated modulation of key metabolic genes, including downregulation of glucose transporter type 4 (GLUT4) and upregulation of PDK4, CPT1, and AMPK, reflecting a metabolic shift toward enhanced fatty acid oxidation and improved insulin sensitivity. In contrast, high-fat and fructose-rich diets promoted proinflammatory gene expression and immune activation, contributing to insulin resistance. Plant-based and vegan dietary patterns were associated with reduced epigenetic aging and improved insulin sensitivity through DNA methylation changes. Targeted interventions, including vitamin D combined with probiotics, dietary fiber, nucleotides, and trace elements such as copper, further demonstrated favorable transcriptional and epigenetic effects linked to improved glycemic control. Collectively, these findings highlight diet-driven modulation of insulin signaling and glucose metabolism at the molecular level and support nutrigenomics-guided precision nutrition as a viable preventive approach for T2DM. Integrating genetic and epigenetic insights into dietary strategies may enable more personalized and effective interventions to curb the growing global burden of type 2 diabetes.

The Frailty Index (FI) is a well-established predictor of accelerated biological aging and a reliable tool for estimating all-cause and cardiovascular disease (CVD) mortality in older adults in the United States. However, its predictive value remains unclear in other U.S. population subgroups. This study aimed to examine the association between FI levels and both all-cause and CVD mortality among patients diagnosed with Cardiovascular-Kidney-Metabolic Syndrome (CKM syndrome). This study utilized the data from the National Health and Nutrition Examination Survey (NHANES 2011-2018), which included 7049 participants with complete information for CKM staging (stages 0-4). We employed multivariate Cox proportional hazards models in conjunction with restricted cubic splines (RCS) to account for potential non-linear relationships in the data. Additionally, segmented Cox proportional hazards models were used to examine the association between FI levels and both all-cause and CVD mortality in the CKM syndrome population. Subgroup analyses stratified by demographic and clinical factors, along with interaction tests, were performed to evaluate the consistency of these associations. After adjusting for potential confounding variables, a nonlinear association was observed between the FI and CKM syndrome. Multivariable Cox regression analysis based on nationally representative data demonstrated that higher FI levels were significantly associated with increased risks of both all-cause and CVD mortality among patients with CKM syndrome. Multivariable analysis indicated a robust association between higher FI levels and the presence of CKM syndrome. Among patients diagnosed with CKM syndrome, each 10-unit increase in the FI was associated with a 54% higher risk of CVD mortality (HR = 1.54, 95% CI: 1.24-1.91; P < 0.001) and a 55% higher risk of all-cause mortality (HR = 1.55; 95% CI: 1.38-1.73, P < 0.0001). Stratified analyses revealed no significant interaction effects between the FI and demographic or clinical factors on mortality outcomes. The results highlight a robust and statistically significant association between FI and increased risk of both all-cause and CVD mortality among individuals with KM syndrome. Notably, FI may serve as a valuable marker for CKM stage stratification and for identifying high-risk patients.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is becoming increasingly prevalent worldwide, particularly among individuals with obesity and type 2 diabetes (T2D). MASLD remains potentially reversible in the early phases but, without timely intervention, it can progress to metabolic dysfunction-associated steatohepatitis (MASH) and hepatic fibrosis, which in turn may advance to cirrhosis and hepatocellular carcinoma over time. With no pharmacological treatments specifically indicated for MASLD, current therapeutic strategies include lifestyle modifications, including dietary modifications. Niacin and its molecular derivatives (collectively belonging to the vitamin B3 group) play a central role in metabolic processes, especially through their involvement in the biosynthesis of the oxidized form of nicotinamide adenine dinucleotide (NAD+). A growing body of preclinical evidence suggests that reduced NAD+ levels are a hallmark of MASLD, and that NAD+ precursors may help attenuate disease progression through multiple mechanisms, including sirtuin 1 (SIRT1)-mediated inhibition of hepatic lipogenesis. Although these findings from experimental models suggest a potential role for niacin and related molecular derivatives as a modulators of MASLD-related pathways, evidence from human studies remains limited and inconsistent. For instance, interventional studies evaluating niacin or molecular derivatives supplementation have reported variable findings, with several trials showing limited meaningful benefits on MASLD-related outcomes. Consequently, further well-designed, controlled trials are needed to clarify therapeutic efficacy, dose-response relationship, and the feasibility of integrating niacin derivatives into dietary or therapeutic strategies aimed at reducing liver fat and improving adverse metabolic outcomes. This review aims to (i) summarize mechanistic insights on the role of niacin as a source of NAD+ on experimental MASLD and (ii) critically evaluate the available human evidence on the effect of supplemental niacin and derivatives in the prevention of MASLD development and its progression to MASH and fibrosis.

Parabiotics (also termed paraprobiotics) are defined as non-viable microbial cells or their components, including peptidoglycans, teichoic acids, surface proteins, that confer health benefits without requiring viability which distinguishes them from traditional probiotics. Their non-viable nature eliminates risks such as microbial translocation, bacteremia, and sepsis, making them suitable for vulnerable populations including immunocompromised, critically ill, paediatric and elderly individuals. In addition, parabiotic exhibit improved thermal stability, extended shelf life, and easier incorporation into functional foods, nutraceuticals, and pharmaceutical formulations without cold-chain requirements. Mechanistically, parabiotics retain immunomodulatory, anti-inflammatory and have barrier-enhancing activities through interactions with host pattern recognition receptors, including Toll-like receptors, modulation of cytokine responses, and reinforcement of gut epithelial integrity. Preclinical and clinical studies support their therapeutic potential such as in case of heat-killed Lactobacillus acidophilus LB (L. acidophilus) has shown efficiency in managing acute paediatric diarrhoea, while heat-inactivated Lacticaseibacillus paracasei PS23 (Lcb. paracasei) has demonstrated improvements in muscle strength and inflammatory markers, including reduced C-reactive protein and interleukin-6 and increased interlukin-10 in elderly individuals. Similarly, inactivated Lactiplantibacillus plantarum (Lpb. plantarum) and Bifidobacterium strains have been associated with benefits in irritable bowel syndrome, atopic dermatitis, respiratory infections, visceral fat reduction, and antibiotic-associated dysbiosis. Synergistic combinations with prebiotics, postbiotics and related bioactives further enhance therapeutic outcomes in inflammatory, metabolic and infectious conditions. Advances in metagenomics, next-generation sequencing, proteomics, metabolomics, CRISPR-Cas systems, and synthetic biology are accelerating strain characterization, functional evaluation, and scalable production. Despite ongoing challenges in standardization and regulated harmonization, parabiotics represent a safe and effective approach for microbiome-targeted interventions. This review synthesizes current evidence on their therapeutic applications, technological advancements, and translational potential, highlighting their role in precision health and next-generation functional nutrition.

The Developmental Origins of Health and Disease (DOHaD) hypothesis asserts that detrimental prenatal conditions, such as dietary deficiencies, may lead to enduring health consequences. Perinatal undernutrition, an important concern during fetal development, may affect growth and metabolic programming, resulting in lasting health implications. Maternal nutrition is crucial in modulating fetal endocrine systems and metabolic functions, influencing the development, blood circulation, and nutrient absorption. The present study examines the impact of perinatal undernutrition on the composition of gut microbiota and metabolite levels in offspring of undernourished dams, using an Albino Wistar rat model. Furthermore, we investigated the combined impact of astaxanthin (AsX) and docosahexaenoic acid (DHA) supplementation on cardiometabolic outcomes in these progenies. Astaxanthin, a powerful antioxidant, and DHA, an omega-3 fatty acid, have shown the ability to favorably alter the gut flora and metabolic pathways. The direct influence of AsX on gut microbiota remains unexplored, whereas DHA's role in fostering beneficial microbes and regulating metabolite production is well documented. The current study used metabolomics and metagenomics to investigate the intricate relationship between metabolites and gut microbiota in health and disease, offering insights into fetal programming and possible strategies to improve offspring health. The results highlight the need to address perinatal undernutrition and enhance gut health through targeted dietary interventions to improve long-term health outcomes.

Protein is a central component of artificial nutrition, yet its optimal dose and timing remain controversial. Provision of both insufficient and excessive protein is associated with adverse outcomes. Inadequate intake promotes negative nitrogen balance, muscle wasting, impaired tissue healing and repair, and increased risk of infection, whereas excessive protein may exceed metabolic capacity, causing azotemia, hepatic or renal strain, and reduced metabolic flexibility - particularly in patients with renal dysfunction. Emerging evidence indicates that the optimal protein dose is strongly influenced by patient-specific characteristics and evolves throughout the course of illness, supporting an individualized, phase-adapted strategy for protein provision rather than a fixed universal target. During early critical illness, catabolism predominates and high protein doses may not be effectively utilized. In contrast, during recovery and stabilization, higher protein targets appear beneficial for restoring lean body mass and functional capacity. This dynamic trajectory underscores the need to abandon universal recommendations in favor of personalized prescriptions. Although instruments such as nitrogen balance, body composition analysis, and indirect calorimetry can provide information about protein dosage, their routine use in clinical practice is limited and interpretation in acute illnesses remains difficult. Pragmatic, bedside strategies and the phenotyping of patients using biomarkers are, therefore, needed to tailor protein provision according to disease stage, organ function, and anabolic capacity. This opinion paper explores mechanistic insights, evidence from clinical trials, and guidelines on protein supplementation, explores biomarker-driven personalization, and highlights ongoing challenges and future research priorities in nutritional therapy.

Diabetic sarcopenia (DS), an emerging diabetes complication, poses an increasing challenge to the elderly population. Shenqi paste (SQP) consists of 8 medicine-food homology substances: Astragalus membranaceus (Fisch.) Bge., Codonopsis pilosula (Franch.) Nannf., Polygonatum sibiricum Red., Dioscorea opposita Thunb., Poria cocos (Schw.) Wolf, Eucommia ulmoides Oliv., Hordeum vulgare L., and Ophiopogon japonicus (L.f.) Ker Gawl. SQP has shown potential benefits for sarcopenia in clinical practice. Its efficacy and safety in DS have not been validated in a randomized controlled trial. This study aimed to evaluate the efficacy, safety, and limitations, and provide insights into methods and strategies for utilizing SQP in DS management. In this randomized, double-blind, placebo-controlled trial, community-dwelling older adults (&#x2265;60 years) with DS and spleen-kidney deficiency syndrome were allocated 1:1 to receive either SQP or placebo paste for 12 weeks. Primary outcomes were skeletal muscle mass index (SMI), handgrip strength, and five-time chair stand test (FCST) duration. Secondary outcomes included health-related scales and biochemical indicators. Assessments were conducted at the baseline (T0), week 6 (T1), and week 12 (T2). Safety evaluation included blood routine, liver and kidney function tests. Intention-to-treat analysis was applied to the primary outcomes data from all participants, with per-protocol analysis for sensitivity. Generalized estimating equations with covariate adjustment and t-tests or Wilcoxon rank-sum tests were used for statistical analysis. Of 90 randomized participants, the SQP group showed greater improvements in handgrip strength (T2: interact p&#xa0;<&#xa0;0.001), SMI (T2: interact p&#xa0;<&#xa0;0.001), and FCST (T2: interact p&#xa0;<&#xa0;0.001) versus control. Secondary outcome measures of 74 participants, including frailty, nutrition, physical activity, sleep quality, depression, and TCM syndrome scores, significantly improved (p&#xa0;<&#xa0;0.05), with significant fasting blood glucose reduction (T2: interact p&#xa0;=&#xa0;0.018) and C-reactive protein decrease (T2: interact p&#xa0;<&#xa0;0.001). There was no statistically significant difference in the change in the difference between the two groups in fasting insulin, glycated hemoglobin and insulin resistance index before and after intervention (p&#xa0;>&#xa0;0.05). Within-group analysis demonstrated significant reductions of SQP group in inflammatory cytokines, and sarcopenia-related biomarkers (p&#xa0;<&#xa0;0.001) post-intervention. No serious adverse events occurred. A 12-week SQP intervention enhanced muscle mass, strength, function, and metabolic and inflammatory profiles in older adults with DS, with good tolerability, supporting its potential as a safe, complementary therapy.

Undernutrition is a type of malnutrition in which there are deficiencies in nutrient intake. It is caused by inadequate dietary intake and disease. Undernutrition contributes toward poor health outcomes of a child, and imposes a financial burden on the child's household. This study aims to determine under-five undernutrition prevalence, its inequality and associated socioeconomic and demographic factors in Uganda. We analyzed secondary data of 2019/2020 Uganda National Panel Survey. From 815 households, selected 815 children under 5 who had complete data on age (months), weight (kilograms), and height (centimeters). This was used for computing the z scores. Based on the World Health Organization reference, we used the z scores to determine the children's nutritional status. We then compared households of malnourished and those of the well-nourished children using the student's t-test and the chi square (&#x3c7;2) test respectively. Among 815 children included in the study, undernutrition prevalence was 16.9% stunted, 6.1% wasted, and 11.8% underweight. This corresponds to catastrophic health expenditure being 1.1%, 1.7%, and 0.7% lower among households with stunted, wasted and underweight children respectively, compared to households with well-nourished children. The distribution was not statistically significant: ( &#x3c7; 2 ( P ) &#x2009;=&#x2009;2.331 (0.312)), ( &#x3c7; 2 ( P ) &#x2009;=&#x2009;0.863 (0.649)), and ( &#x3c7; 2 ( P ) &#x2009;=&#x2009;0.335 (0.846)), respectively. The odds of undernutrition didn't differ by nutritional status, but undernourished children had significantly higher transport expenses. MoH should invest in community healthcare services to reduce these costs.

Early feeding of starter is an effective strategy for modulating gastrointestinal microbiota in newborn calves. However, the effects of starter nutrient composition on calf gut microbiota vary significantly. Although both fiber and starch are essential for early calf nutrition, each has distinct advantages and disadvantages. This study investigated how high-starch and high-fiber diets influence growth performance, hindgut health, and microbiota in calves. Two groups of calves were fed experimental starters with distinct nutrient compositions: a high-starch (HS, n = 8) diet containing 40.4% starch and 13.3% NDF, and a high-fiber (HF, n = 7) diet containing 18.8% starch and 30.5% NDF (DM basis). The experiment spanned calf ages 14 to 63 d, with weekly BW and body size measurements using calibrated scales and measuring tape. Serum was collected via jugular venipuncture for metabolic marker analysis. At trial end, animals were slaughtered to collect hindgut tissues and contents for immunoblotting, metagenomic sequencing, and metabolite analysis. We identified a fundamental trade-off that HS feeding shaped a Bifidobacterium-dominated enterotype, correlating with superior growth performance. In contrast, HF feeding selected for a Bacteroides-dominated, more mature microbiota and significantly enhanced gut barrier integrity by upregulating key tight junction proteins (ZO-1, claudin-1, and E-cadherin). Multiomics integration revealed that this trade-off was underpinned by different microbial metabolic pathways. The HS hindgut was enriched in enzymes and metabolites for carbohydrate and AA fermentation, driving growth. Conversely, the HF hindgut exhibited enhanced enzymatic capacity for fiber degradation (e.g., starch phosphorylase) and a metabolic profile favoring arginine biosynthesis and acetate production, which supported barrier function. This functional divergence was further evidenced in distinct short-chain fatty acid (SCFA) profiles. The HF group exhibited significantly elevated acetate and a trend for higher total SCFA concentration, whereas the HS group showed increased branched-chain fatty acids (isovalerate) and a trend toward higher butyrate and valerate proportions. Our findings provide a mechanistic model linking dietary carbohydrate source to a fundamental choice between growth optimization and gastrointestinal health in preweaning calves, offering novel insights for targeted nutritional strategies.

Background: cardiovascular disease and metabolic syndrome are major contributors to global morbidity and mortality. Dyslipidaemia plays a central role in their pathogenesis. Olive-derived polyphenols, particularly oleuropein and hydroxytyrosol, have gained attention for their potential lipid-modulating and vascular-protective effects. Objective: This narrative review synthesizes clinical and mechanistic evidence on the effects of olive leaf and olive oil polyphenols on blood lipid profiles and cardiovascular risk markers in both healthy and at-risk populations. Methods: clinical studies using standardized olive leaf extracts (OLE) or olive oil preparations with defined phenolic content were included. Multi-ingredient formulations containing additional bioactive compounds were excluded to isolate the effects of olive-derived polyphenols. Evidence was categorized by population (healthy, cardiovascular risk, overweight/obese, hyperlipidaemic) and complemented by mechanistic insights from animal and cell-based studies. Results: in healthy individuals, olive-derived polyphenols mainly improved oxidative and vascular markers, with little effect on absolute lipid levels. In individuals with elevated cardiovascular risk, reductions in low-density lipoprotein cholesterol, total cholesterol, triglycerides, and oxidised low-density lipoprotein were more consistently observed. Overweight and obese participants showed no lipid changes at the studied doses, while postmenopausal and mildly hyperlipidaemic adults displayed modest short-term improvements and larger lipid reductions with longer supplementation. Mechanistic studies indicate that olive polyphenols influence lipid metabolism and vascular function through AMPK activation, suppression of SREBP-1c, modulation of PPAR pathways, enhancement of antioxidant defences via Nrf2 signalling, and attenuation of inflammatory pathways including NF-&#x3ba;B and MAPK. Conclusion: overall, current evidence indicates that olive leaf and olive oil polyphenols can beneficially modulate lipid parameters, oxidative stress, inflammation, and vascular function. The strongest and most consistent lipid-related effects are observed in individuals with elevated cardiovascular risk and in long-duration interventions in hyperlipidaemic postmenopausal women. While mechanistic studies support multiple pathways relevant to lipid regulation, long-term standardized clinical trials with well-characterized polyphenol compositions are needed to confirm efficacy and identify optimal dosing strategies across different metabolic phenotypes.

Type 2 diabetes (T2D) is a heterogeneous metabolic disorder in which environmental exposures interact with host biology to drive insulin resistance and progressive &#x3b2;-cell dysfunction. This review synthesizes recent advances showing how the gut microbiome mediates these processes across multiple levels of resolution. First, large-scale shotgun metagenomic studies consistently identify a reproducible T2D-associated signature characterized by depletion of short-chain fatty acid-producing taxa and enrichment of opportunistic, pro-inflammatory microorganisms, while highlighting the importance of controlling for major confounders such as adiposity and glucose-lowering medications. Second, functional profiling and metabolomics link microbial community shifts to coordinated pathway changes-including reduced short-chain fatty acid and secondary bile acid production and increased endotoxin- and branched-chain amino acid-related metabolism-that influence gut barrier integrity, inflammatory tone, insulin sensitivity, and pancreatic &#x3b2;-cell function. Third, we discuss how integrative multi-omics (metagenomics, metatranscriptomics, proteomics, and metabolomics) can connect microbial genetic potential to in vivo activity and circulating metabolites, while introducing key challenges such as temporal variability, anatomical heterogeneity, and "dark matter" in gene and metabolite annotation. Fourth, strain-resolved analyses reveal that many disease-associated functions are carried by specific lineages within species, refining microbial targets and helping explain inconsistent species-level associations. Fifth, we summarize how diet shapes microbial ecology and function-supporting microbiome-informed precision nutrition-and highlight emerging evidence beyond bacteria, including viral and fungal community components. Finally, we outline translational opportunities and evidence gaps, emphasizing the need for diverse longitudinal cohorts, mechanistic validation, and well-controlled interventional trials to evaluate microbiome-directed strategies for T2D prevention and treatment.

BeaT-2/Sugarburner is a nutritional supplement based on a co-existing microbial consortium of bacterial strains. The purpose of this study was to investigate potential beneficial effects of the supplement versus placebo on glycemic control and on biomarkers of inflammation, insulin resistance and &#xdf;-cell dysfunction. A total of 40 Patients with type 2 diabetes (31 male, 9 female, age:65.5&#x2009;&#xb1;&#x2009;8.0&#x2009;years, BMI: 33.6&#x2009;&#xb1;&#x2009;5.5&#x2009;kg/m&#xb2;, HbA1c: 7.2&#x2009;&#xb1;&#x2009;0.9%) were included into the study. They were randomized to receive 2 capsules of either BeaT-2 or placebo once daily for 6&#x2009;weeks. Observation parameters were time in normoglycemia as assessed by continuous glucose monitoring, and biomarkers of glycemic control, &#xdf;-cell function, insulin resistance and chronic systemic inflammation. Time in range was stable with BeaT-2 between weeks 0 and 2 versus weeks 4 and 6, while it slightly impaired with placebo (-4%, n.s.). At endpoint, there were significant improvements versus baseline with BeaT-2, but not with placebo for biomarkers of glycemic control (BeaT-2 vs Placebo, HbA1c: -0.3% vs 0.1%, fasting glucose: -14% vs +8%, both P&#x2009;<&#x2009;.05), insulin resistance (insulin: -17% vs +14%, HOMA-IR: -26% vs +21%, both P&#x2009;<&#x2009;.05), &#xdf;-cell dysfunction (intact proinsulin: -40% vs -2%, P&#x2009;<&#x2009;.05) and chronic systemic inflammation (adiponectin: +8% vs -8%; P&#x2009;<&#x2009;.05, hsCRP: -31% vs +27%, n.s.). In addition, observed changes in the lipid profiles and other parameters of metabolic syndrome were more favorable with BeaT-2 than with placebo. There were no differences between the groups with respect to number and type of adverse events. The results observed with BeaT-2 were comprehensively indicative for improvements in the cardiometabolic situation. BeaT-2 may be a valuable supplement to any existing treatment combination in patients with type 2 diabetes.

The proper structure and source of dietary carbohydrates are vital for farmed fish health, yet their metabolic responses to varied carbohydrates are not clear. To explore fish metabolic responses to varied carbohydrates, Nile tilapia was fed with five different carbohydrate diets for eight weeks. The results showed that polysaccharides significantly enhanced the growth performance of fish (P&#xa0;<&#xa0;0.05). The fish fed with polysaccharides showed lower serum glucose, pyruvate and lactate, while their liver glucose uptake and catabolic capacity were significantly enhanced (P&#xa0;<&#xa0;0.05). Furthermore, the PDK4-PDHE1&#x3b1; axis, which linked glycolysis to the TCA cycle, exhibited a stronger response to polysaccharides, particularly in the corn starch group. The total lipid of the whole fish, as well as the TG in the liver and serum, were significantly elevated in the fish fed with wheat and tapioca starch (P&#xa0;<&#xa0;0.05). Additionally, the fish fed with wheat and tapioca starch exhibited a significant higher expression of PPAR&#x3b3;, DGAT and FAS (P&#xa0;<&#xa0;0.05). The serum levels of AST and ALT, as well as the liver MDA content, significantly decreased in the fish fed with polysaccharides (P&#xa0;<&#xa0;0.05). Meanwhile, the expression levels of pro-inflammatory (TNF&#x3b1; and IL12) and apoptosis (caspase8 and caspase9) -related genes in the liver were significantly downregulated, while the antioxidant capacity markedly increased (P&#xa0;<&#xa0;0.05). The total protein of the whole fish, muscle protein content, and muscle fiber diameter of fish fed polysaccharides were significantly increased, particularly in the corn starch group (P&#xa0;<&#xa0;0.05). Furthermore, the fish fed with polysaccharides exhibited stronger mTOR signaling response and higher protein synthesis capacity in the muscle, particularly in the corn starch group (P&#xa0;<&#xa0;0.05). This study demonstrated that the PDK4-PDHE1&#x3b1; axis and mTOR exhibit a stronger response to polysaccharides, boosting carbohydrate breakdown and protein synthesis for growth. PPAR&#x3b3; responds more robustly to wheat and tapioca starch, facilitating the esterification of free fatty acids into TG, which reduced lipid toxicity and maintained liver health.

Different soil amendments differentially affect selenium (Se) and cadmium (Cd) bioavailability in soils where Se and Cd naturally co-occur, and the underlying regulatory mechanisms remain unclear. This study examined how calcium superphosphate (P), biochar (BC), and organic manure (OM) regulate Se/Cd migration and transformation in a seleniferous soil-rapeseed system. P significantly reduced Se accumulation with little effect on Cd; BC enhanced Se uptake but reduced Cd; and OM reduced both. All amendments decreased microbial-derived humic-like components (C1) and increased fulvic-like, terrestrial humic-like, and highly humified humic acid components. OM induced the greatest enrichment of Actinobacteriota, followed by BC and P. Metabolomics revealed that P activated lipid metabolism and plant growth pathways; BC enhanced amino acid metabolism, promoting the transformation of DOM-bound Se; OM stimulated microbial metabolism, reducing C1 and enhancing Actinobacteriota (particularly Promicromonospora)-mediated Se/Cd immobilization. These findings demonstrate that amendments regulate Se/Cd bioavailability through DOM-microbe-metabolite interactions. Amendment selection should be based on the Se/Cd bioavailability in the target soil.

This study aimed to compare mortality risks among patients with stage 2 cardiovascular-kidney-metabolic syndrome (CKM) across different multimorbidity states. Furthermore, it investigated whether sufficient serum vitamin D (&#x2265;75&#x2009;nmol/L) modulates the association between multimorbidity and mortality. Using data from the 2001-2018 National Health and Nutrition Examination Survey (NHANES), we conducted a retrospective cohort study of 12,406 eligible patients. Among these patients, 913 died from all causes, and 223 died due to CVD. Survey-weighted Cox proportional hazards regression analyses revealed that compared to group 1 multimorbidity, groups 2 (all-cause mortality HR = 1.79; CVD mortality HR = 2.10), 3 (all-cause HR = 1.89; CVD HR = 1.76), and 4 (all-cause HR = 2.55; CVD HR = 3.97) had significantly increased mortality risks. Notably, sufficient serum 25-hydroxyvitamin D [25(OH)D] levels demonstrated a potential antagonistic effect on multimorbidity-related mortality, particularly for CVD. These findings indicate that maintaining adequate VD in stage 2 CKM patients may mitigate mortality risks associated with multimorbidity progression, offering insights for improving cardiovascular outcomes. People who have combinations of heart, kidney, and metabolic diseases, collectively referred to as cardiovascular-kidney-metabolic (CKM) syndrome, are at higher risk of dying earlier, especially when they have several chronic conditions at the same time (multimorbidity). Vitamin D, which the body produces through sunlight exposure and obtains from food, may influence how these diseases interact. In this study, we analyzed data from more than 12,000 adults in the U.S. National Health and Nutrition Examination Survey (NHANES) collected between 2001 and 2018. All participants were at stage 2 of CKM syndrome, meaning they had metabolic risk factors or moderate chronic kidney disease but no known cardiovascular disease. We found that individuals with a greater number of coexisting diseases had higher risks of death from any cause and from cardiovascular disease. However, participants with adequate vitamin D levels (at least 75&#x2009;nmol/L) showed lower mortality risks, suggesting that maintaining sufficient vitamin D may help reduce some of the harmful effects of multimorbidity. These findings indicate that assessing and managing vitamin D levels could become an important part of early care for people with CKM syndrome. Further studies are needed to determine whether vitamin D supplementation can directly improve survival outcomes.

Monascus sp. NP1 is a significant filamentous fungus with valuable properties for food industries. Initially isolated from the fermented rice product ang-kak, this strain is known for its ability to produce natural pigments. In this study, we therefore sequenced its genome together with the 26S rRNA D1/D2 domain and ITS fragment for identifying species of Monascus sp. NP1, and further conducted functional annotations of its overall genes related to metabolic capability and growth adaptation using comparative genomics. As a result, promisingly, the NP1 strain was identified as Monascus purpureus with the genome sequences, which was shown to be 23.54 Mb with a GC content of 49.01%. Genome annotation predicted 8031 protein-encoding genes. Comparative genomics between NP1 and 11 other related strains revealed 6024 core groups, 2204 accessory groups, and 5 strain-specific groups. Metabolic pathway analysis promisingly showed carbohydrate metabolism as the most enriched category, particularly central carbon metabolism involving key precursors, e.g., acetyl-CoA and pyruvate that support energy generation and the biosynthesis of pigments, fatty acids, and lipids. These findings highlighted the metabolic versatility and adaptive growth potential of M. purpureus NP1. This study provides key genetic insights into the cellular functions of M. purpureus NP1, laying the groundwork for exploring metabolic properties. It offers a comprehensive understanding for developing targeted applications of M. purpureus NP1 as an alternative fungal cell factory in food and nutrition.

Hyperuricemia (HUA) is a metabolic disorder and a major cause of gout in geese, commonly exacerbated by concentrate diets rich in protein and calcium. Elevated uric acid (UA), a potent pro-oxidant, contributes to renal injury and is strongly influenced by dietary composition and gut microbiota. Therefore, research for natural feed ingredients that can regulate UA homeostasis and oxidative stress is particularly essential. Perennial ryegrass, a fiber-rich forage containing abundant minerals and antioxidant flavonoids, may mitigate these adverse effects, however its renoprotective potential in goslings remains unclear. This study investigated the protective effects of perennial ryegrass against UA-induced oxidative stress and renal damage in goslings. High-through 16S rRNA and LC-MS metabolomics were performed to determine the effect of ryegrass on the gut microbiota-metabolite axis in goslings. Biochemical indexes, histopathology, immunofluorescence, gene expressions, and western blotting were used to observe the renoprotective potential of ryegrass. Ryegrass significantly lowered serum UA and creatinine levels (p < 0.05) by upregulating renal UA-excreting transporters (ABCG2, OAT1 and OAT3) and downregulating UA-reabsorbing transporters (URAT1 and GLUT9). Histopathology and microbial profiling revealed that ryegrass reduced tubular damage, fibrosis, and immune cell infiltration, accompanied by enrichment of short chain fatty acid-producing bacterial taxa. Transcriptional, protein, and immunofluorescence analysis demonstrated that ryegrass suppressed inflammatory cytokines (IL-1&#x3b2;, IL-18, TNF-&#x3b1;) through inhibition of the NLRP3/caspase-1/Keap1 axis, likely related to decreased renal UA burden. In parallel, it strengthened antioxidant defenses by upregulating Nrf2, which increased GSH-Px, CAT, and SOD activities and lowered MDA and ROS accumulation. Metabolomics further demonstrated higher levels of antioxidant metabolites (caffeic acid, kaempferol, skimmin, quercetin, and ferulic acid) in ryegrass-fed goslings relative to the concentrate-fed group. These findings highlight the renoprotective potential of perennial ryegrass in alleviating UA-induced oxidative renal injury and provide new insights into its value as a functional forage in the geese industry.

Methionine is an essential amino acid that plays a vital role in animal growth and development, lipid metabolism, intestinal health, and 1-carbon metabolism as a primary methyl donor. Emerging evidence indicates that maternal methionine status exerts long-term effects on offspring growth, metabolism, and health through developmental programming, largely mediated by epigenetic mechanisms. These mechanisms primarily involve alterations in deoxyribonucleic acid methylation, histone modifications, and related epigenetic regulatory networks that modulate gene expression during critical periods of embryonic and postnatal development. This review highlights recent advances in the physiological functions of methionine and the epigenetic mechanisms underlying maternal methionine-mediated regulation of offspring development, with particular emphasis on findings from animal models. We highlight how variations in maternal methionine status influence offspring phenotypes by reshaping epigenetic landscapes associated with growth, metabolic homeostasis, and tissue development. By integrating current evidence from nutritional, molecular, and epigenetic perspectives, this review aims to provide a comprehensive theoretical framework for optimizing maternal-offspring methionine nutrition strategies and to offer insights for improving offspring health and productivity in both animals and humans.