搜索结果：Nutrition and metabolic insights

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.

India's escalating burden of obesity and metabolic disease is characterized by a distinctive "thin-fat" phenotype, in which individuals with normal or near-normal body mass index exhibit disproportionate visceral adiposity, reduced skeletal muscle mass, and heightened susceptibility to insulin resistance. Conventional obesity models centered primarily on caloric imbalance fail to adequately explain this pattern, underscoring the need for a more integrative pathophysiological framework. Emerging evidence implicates gut microbiome dysbiosis, impaired fermentation of dietary fibers, reduced short-chain fatty acid (SCFA) signaling, altered bile acid metabolism, metabolic endotoxemia, and dysregulated adipose tissue crosstalk as key contributors to metabolic vulnerability in South Asian populations. This commentary synthesizes mechanistic insights into the gut-metabolic axis and examines their relevance to India's phenotype-specific challenges. Key pathways, including SCFA-mediated incretin secretion, Toll-like receptor 4 (TLR4)-driven inflammatory signaling, angiopoietin-like protein 4 (ANGPTL4)-mediated lipid partitioning, and microbiota-dependent bile acid biotransformation, are discussed as interconnected drivers of metabolic dysfunction. Emerging clinical evidence from randomized controlled trials evaluating synbiotic and prebiotic-botanical formulations is also discussed, highlighting their potential benefits as adjuncts to lifestyle modification. Given India's dietary patterns and widespread deficiency of fermentable fiber intake, synbiotics may represent a scalable and biologically coherent strategy to support metabolic health. However, heterogeneity of formulations, interindividual microbiome variability, and limited long-term outcome data necessitate cautious interpretation. Advancing precision microbiome-targeted interventions will require population-specific research, multi-omics integration, and rigorous clinical evaluation.

Mitochondrial dysfunction and redox imbalance are key features of aging that drive cellular senescence, metabolic decline, and tissue degeneration. 4-N-furfurylcytosine (FC), a cytosine derivative with redox-modulating properties, has been proposed to counteract age-associated oxidative damage; however, its effects in mammalian aging remain unexplored. The anti-aging potential of FC was investigated using a translational approach integrating in vitro and in vivo models. Human fibroblasts (MRC-5) and keratinocytes (HaCaT) subjected to physiological and stress-induced senescence were used to assess mitochondrial function, redox balance, and proteostasis, while aged C57BL/6J mice, long-term supplemented with FC were evaluated for systemic metabolic, molecular, and behavioral outcomes. FC enhanced cell survival and mitigated key hallmarks of senescence, including β-galactosidase activity and p16 expression. Moreover, FC reduced intracellular reactive oxygen species and oxidative damage, as evidenced by decreased levels of 8-oxodG, protein carbonyls, and lipid peroxidation. FC improved mitochondrial membrane polarization and increased ATP levels while reducing oxygen consumption, indicating an altered bioenergetic state. Proteomic profiling revealed enrichment of pathways related to mitochondrial maintenance, antioxidant defense, and proteostasis, consistent with enhanced metabolic adaptability. In aged mice, FC supplementation preserved lean body mass, improved coordination and endurance, stabilized lipid and glucose metabolism, maintained telomere integrity, increased mtDNA:nDNA ratio, and reduced systemic oxidative stress markers, indicating delayed molecular aging and preserved mitochondrial function without overt adverse effects detected in the measured readouts. 4-N-furfurylcytosine modulates redox- and mitochondria-associated aging phenotypes in cellular and mouse models, with effects consistent with remodeling of mitochondrial homeostasis and improved resilience to oxidative stress. These findings support FC as a promising candidate for further investigation as a modulator of aging-related processes.

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.

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-κB 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.

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.

Sarcopenia is an age-related syndrome characterized by the progressive loss of skeletal muscle mass, strength, and function, significantly impairing older adults' independence and quality of life. Given their anti-inflammatory, antioxidant, and metabolic regulatory properties, n-3 polyunsaturated fatty acids (n-3 PUFAs) have emerged as a promising nutritional strategy to mitigate this muscle degeneration. This review systematically synthesizes existing evidence regarding the association between n-3 PUFAs and sarcopenia. To capture the relevant literature, we searched PubMed, Web of Science, CNKI, and Wanfang Data using a combination of subject headings and free-text terms. We supplemented primary search terms-such as "n-3 polyunsaturated fatty acids," "omega-3 fatty acids," "sarcopenia," and "muscle mass"-with mechanism-related keywords like "inflammation," "muscle satellite cells," and "oxidative stress." We also manually screened the reference lists of the included literature. Our inclusion criteria encompassed interventional studies, observational studies, and high-quality reviews, while excluding conference abstracts, duplicate publications, and studies with incomplete data. This review first outlines the established biological mechanisms linking n-3 PUFAs to the pathological progression of sarcopenia, specifically detailing how these fatty acids improve muscle satellite cell function, suppress inflammation and oxidative stress, and ameliorate metabolic disorders. Next, we critically evaluate recent clinical studies and reviews, analyzing sources of study heterogeneity such as variations in sample size, intervention dose and duration, outcome measures, and baseline participant characteristics. We also highlight current research hotspots-including specialized pro-resolving mediators (SPMs), the gut-organ axis, combined interventions, and precision nutrition strategies-while emphasizing the functional differences between EPA and DHA to guide future intervention designs. Current evidence indicates that while n-3 PUFA supplementation can improve muscle strength and physical performance in older adults, its effects on muscle mass remain inconsistent. Addressing key research gaps, particularly the lack of standardized core outcome measures and unclear dose-response relationships, is critical. Ultimately, future research must prioritize developing high-bioavailability formulations, conducting personalized trials based on baseline n-3 PUFA status, and deepening investigations into inter-organ networks to translate these nutritional insights into effective sarcopenia prevention and management strategies.

Early-life growth patterns are increasingly recognised as critical determinants of long-term health trajectories. A substantial body of evidence links suboptimal growth during early development with an elevated risk of chronic, age-related disorders in adulthood. In particular, maternal undernutrition leading to foetal growth restriction, especially when followed by rapid postnatal catch-up growth, markedly increases susceptibility to cardiometabolic and other degenerative diseases later in life. Conversely, maternal overnutrition and associated metabolic disturbances also exert lasting effects on offspring physiology, predisposing individuals to conditions such as cardiovascular disease, type-2 diabetes, and metabolic syndrome. Emerging mechanistic insights highlight redox imbalance as central mediator of maternal nutrition-induced developmental programming. Perturbations in oxidative homeostasis during critical windows of development can induce persistent alterations in cellular energetics, metabolic regulation, and tissue function, thereby accelerating biological ageing processes. In parallel, accumulating evidence implicates epigenetic modifications, including changes in DNA methylation, histone modifications, and non-coding RNA expression, as key mechanisms through which maternal nutritional status exerts durable effects on gene expression and disease susceptibility.

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a common chronic liver disorder linked to obesity, insulin resistance, and dyslipidemia. Nutrition plays a central role in modulating hepatic lipid metabolism, oxidative stress, and inflammation, yet practical, evidence-based dietary strategies remain limited. This study aimed to develop Mediterranean diet-based meal plans with varying macronutrient compositions and to characterize their nutritional profiles, as well as to evaluate them using established nutritional indices and diet score calculations, such as the Dietary Inflammatory Index, Dietary Antioxidant Index, and dietary lipid indices. Methods: Clinical practice guidelines (CPGs) from various academic and professional organizations were reviewed to assess current non-pharmacological treatments for MASLD, with a focus on determining whether the Mediterranean diet is the most recommended dietary pattern. Traditional, low-carbohydrate, and low-fat MedDiet patterns were translated into food-based meal plans. A 7-day meal plan was developed and analyzed for nutrient composition, then evaluated using the Dietary Inflammatory Index (DII), Dietary Antioxidant Index (DAI), Dietary Lipophilic Index (DLI), and Dietary Lipophilic Load (DLL). A Western diet (WD) that is characterized by ultra-processed food (UPF) was included as a comparative reference. Results: The validated dietary score calculations showed that all MedDiet patterns demonstrated consistently low DII scores (-2.00 to -2.81) and high DAI scores (3 to 20.03), whereas the WD showed high DII scores (5.0 to 6.09) and low DAI scores (-12.47 to -17.99). Despite these variations in macronutrients, the menu developed in the study on three MedDiet patterns showed negative DII and positive DAI scores. When comparing the traditional MedDiet with the WD, which have similar macronutrient distributions, the WD was characterized by less favorable DII and DAI scores. Conclusions: This study provides a descriptive, guideline-informed framework for Mediterranean diet-based meal plans with varying macronutrient compositions. Utilizing DII, DAI, DLI, and DLL offers a potential framework for designing dietary interventions. Further validation through clinical studies is needed to justify the potential for practical and digital translation. Nevertheless, the study provides initial insights that may inform future research on nutritional approaches for MASLD integrating dietary indices.

Type 2 diabetes (T2D) is a heterogeneous metabolic disorder in which environmental exposures interact with host biology to drive insulin resistance and progressive β-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 β-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.

Maternal obesity is a major public health challenge that elevates pregnancy risks and predisposes offspring to lifelong metabolic disorders. Nutrition, as a modifiable determinant of the intrauterine environment, offers opportunities to interrupt this intergenerational cycle. This review synthesizes evidence on polyphenols, vitamins, omega-3 fatty acids, dietary fiber, probiotics, prebiotics, whole grains, and iron, highlighting underlying mechanisms and translational implications for maternal and offspring health. Preclinical studies demonstrate that these interventions improve maternal metabolism, modulate placental function, regulate gut microbiota, alter breast milk composition, and influence epigenetic programming. Clinical evidence is relatively strong for folic acid and vitamin D, whereas evidence for dietary fiber is emerging, with long-term offspring outcomes still insufficiently investigated. Polyphenols and omega-3 fatty acids exert antioxidant and anti-inflammatory effects, but translation is constrained by low bioavailability and limited safety data. Probiotics and prebiotics show potential in modulating maternal-infant gut health, yet trial outcomes are inconsistent and strain-specific. Whole grains and fortified foods may represent feasible options for population-level implementation, although robust longitudinal studies in obese pregnancies are still lacking. Dietary interventions hold promise for mitigating maternal obesity by improving metabolism, reducing inflammation, supporting placental function, and modulating gut microbiota, breast milk composition, and epigenetic programming. However, evidence is largely preclinical and long-term human data are limited. Future research should prioritize well-designed clinical trials and personalized approaches tailored to maternal phenotype and nutritional status to enable effective, scalable strategies for breaking the intergenerational cycle of obesity.

Plant-based milks have been increasing in popularity amongst Australian consumers, concurrent with a decrease in cow's milk consumption. Given the key role of cow's milk in Australian diets, it is necessary to understand the motivations behind this consumer behaviour and investigate the nutritional implications associated with this shift in dietary choice. Adults, including both omnivores and purposefully targeted vegan individuals, were recruited via social media to complete an online survey and two 24-h dietary recalls using the online Intake24 dietary assessment programme. The survey explored milk type choice and participant perceptions of the health and environmental impact of plant-based milks. Respondents were divided into groups based on whether they reported to consume or not consume dairy products in the survey. Survey and dietary intake data were then compared between these two groups. Of the 217 survey responses received (n&#x2009;=&#x2009;74 dairy and n&#x2009;=&#x2009;143 non-dairy consumers), soy, almond and oat plant-based milks were the most popular choices. The primary drivers behind milk type choice were animal rights, self-reported adverse health symptoms and environmental concerns. Additionally, non-dairy consumers were more likely to perceive these products as healthier and better for the environment than cow's milk. Dietary intake data identified that overall non-dairy consumers had significantly lower intakes of saturated fat, iodine and vitamin B12 (14.9 vs. 21.9&#x2009;g/day; p&#x2009;=&#x2009;0.001, 70.8 vs. 128.8&#x2009;&#x3bc;g/day; p&#x2009;<&#x2009;0.001 and 0.9 vs. 3.0&#x2009;&#x3bc;g/day; p&#x2009;<&#x2009;0.001, respectively) and higher amounts of dietary fibre (27.2 vs. 21.3&#x2009;g/day; p&#x2009;=&#x2009;0.008) compared to dairy consumers. This study provides novel insights into the motivations to consume, and perceptions of the healthfulness, plant-based milk in Australia and identified that non-dairy consumers may be at increased risk of iodine and vitamin B12 deficiency.

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.

INTRODUCTION: Long-term weight loss after metabolic bariatric surgery largely depends on patients&#x2019; adherence to postoperative dietary and lifestyle recommendations, yet tools to clinically assess such adherence across different cultures remain limited. The Eating Behavior after Bariatric Surgery scale is a contemporary measurement tool developed to assess postoperative behavioral patterns, including nutrition-related behaviors, self-monitoring, and physical activity. This study aimed to translate this scale into Turkish and to explore its clinical relevance by examining associations with postoperative weight-related outcomes. METHODS: This cross-sectional study included 298 patients who had undergone metabolic bariatric surgery. Sociodemographic and surgical characteristics, pre- and postoperative weight measures, and subscale scores were collected. The translation and cultural adaptation of the scale involved forward&#x2013;back translation and expert review, without formal psychometric validation. Relationships between the subscale scores and weight-related outcomes were examined using correlation analyses and multiple linear regression to evaluate clinical relevance. RESULTS: Mean total weight loss was 33.5&#x2009;&#xb1;&#x2009;16.2&#xa0;kg. The subscale scores indicated highest adherence for drink consumption (5.3&#x2009;&#xb1;&#x2009;0.9) and lowest for general behaviors (3.3&#x2009;&#xb1;&#x2009;1.4). Correlation analyses showed significant associations between the subscales and weight-related outcomes. In regression analysis, preoperative weight and time since surgery positively predicted postoperative total weight loss percentage, whereas food consumption adherence was negatively associated with postoperative total weight loss percentage (R&#xb2;=0.245; p&#x2009;<&#x2009;0.01). CONCLUSION: In this study, higher adherence scores in the food consumption domain were unexpectedly associated with lower postoperative total weight loss, highlighting the complex relationship between self-reported eating behaviors and weight outcomes. These findings suggest that the Turkish version of the scale may provide clinically informative insights into postoperative eating behaviors, while highlighting the complex relationship between self-reported adherence and weight outcomes. KEY POINTS: The Turkish version of the EBBS enables a structured clinical assessment of postoperative eating and lifestyle behaviors in patients who have undergone metabolic bariatric surgery. EBBS domain scores demonstrated domain-specific associations with postoperative weight-related outcomes, supporting their clinical relevance rather than formal psychometric validity. Higher self-reported adherence in the food consumption domain was unexpectedly associated with lower postoperative total weight loss, underscoring the complex and non-linear relationship between self-reported eating behaviors and weight outcomes after surgery.

Increasing concerns over excessive agrochemical use, the emergence of resistant phytopathogens, and the impacts of climate variability on crop productivity have increased interest in plant growth promoting rhizobacteria (PGPR) as promising biological alternatives for sustainable crop production. Pseudomonas spp. are among the most extensively studied PGPR due to their remarkable metabolic diversity, strong rhizosphere colonization, and multifunctional roles in enhancing plant nutrition, improving stress tolerance, and suppressing plant diseases. These Gram-negative bacteria enhance plant growth through diverse direct and indirect mechanisms, including biological nitrogen fixation or stimulation of nitrogen fixation in&#xa0;co-existing&#xa0;diazotrophs, phosphate solubilization, siderophore-mediated iron acquisition,&#xa0;nutrient and niche&#xa0;competition with pathogens, secretion of antimicrobial metabolites, and activation of induced systemic resistance in plants. Recent advances in omics technologies have improved understanding of the mechanisms underlying Pseudomonas mediated plant nutrition and biocontrol. However, these insights remain fragmented across the literature, limiting a comprehensive understanding of Pseudomonas-plant interactions. This review synthesizes current knowledge on nutrient mobilization, siderophore activity, antimicrobial metabolite production, and induced plant defense responses associated with beneficial Pseudomonas spp. Emphasis is placed on how these mechanisms collectively enhance plant productivity, stress tolerance, and disease resistance, highlighting the potential of Pseudomonas spp. as sustainable biofertilizers and biopesticides.

Chronic kidney disease (CKD) is characterized by systemic metabolic disturbances and oxidative stress. Nutritional interventions using bioactive compounds such as sulforaphane (SFN) may represent a promising adjuvant strategy to attenuate these alterations. This study evaluated the effects of SFN supplementation on the untargeted metabolomic profile of non-dialysis CKD patients. A randomized, placebo-controlled clinical trial was conducted in 14 patients with CKD stages 3-5 who received either 400 &#xb5;g per day of SFN or placebo for 30 days. Serum samples were analyzed using proton nuclear magnetic resonance (1H NMR) spectroscopy to identify metabolomic alterations and their correlations with markers of oxidative stress, inflammation, and gene expression. SFN supplementation tended to reduce 2-hydroxyisovalerate and glycerol levels, metabolites associated with insulin resistance and oxidative stress, and attenuated methanol elevation. Correlations were identified between heme oxygenase-1 (HO-1) and several amino acids, and between NRF2 and glycerol, suggesting an interplay between amino acid metabolism and antioxidant defense. Overall, SFN modulated the metabolomic profile of CKD patients, particularly metabolites related to mitochondrial function, lipid metabolism, and oxidative balance. These findings demonstrate that NMR-based metabolomics is a powerful non-invasive approach for elucidating the molecular effects of nutritional therapies in CKD and support SFN as a potential nutraceutical strategy in renal care.

Taurine is a non-proteinogenic &#x3b2;-amino acid that plays fundamental roles in cellular homeostasis. Although it is the most abundant free amino acid in many tissues, the full spectrum of its molecular functions has only recently begun to be elucidated. Taurine supplementation has shown promising outcomes in human studies, with emerging relevance in precision nutrition and the prevention of metabolic and age-related diseases. In this review, we summarize the current knowledge on taurine's molecular mechanisms, including its roles in antioxidant defense, anti-inflammatory signaling, calcium regulation, mitochondrial function, and lipid metabolism. We integrate mechanistic insights with evidence from clinical and nutritional studies examining taurine supplementation in the contexts of oxidative stress, inflammation, metabolic syndrome, and physical performance. Increasing data suggest that taurine can modulate key pathways linked to metabolism, inflammation, and healthy aging. Physiological synthesis and dietary intake appear sufficient to maintain basal health; however, human trials indicate that supplementation of 1-6 g day-1 may further promote metabolic resilience and mitochondrial function without adverse effects. Collectively, these findings position taurine as a promising dietary compound at the interface of metabolism, inflammation, and aging, highlighting its potential as a modulator of healthspan within precision nutrition strategies.

In the EXSCEL trial, exenatide did not reduce major adverse cardiovascular events (MACE), but heterogeneity of benefit and the role of cardiac biomarkers remain uncertain. We evaluated the prognostic value of baseline and 1-year changes in N-terminal pro B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin I (cTnI), and whether baseline biomarker concentrations modified exenatide effects. EXSCEL randomized 14,752 adults with type 2 diabetes to exenatide 2 mg weekly (EQW) or placebo. In a biomarker cohort, 4,292 participants had serial NT-proBNP or cTnI at baseline and 1 year. Biomarkers were log transformed and Cox models related baseline concentrations and 1-year change to MACE, all-cause mortality (ACM), cardiovascular (CV) death, hospitalization for heart failure (hHF), adjusting for clinical covariates and the alternate biomarker. Treatment interaction was tested with biomarker by treatment terms. Over median 1,480 days follow-up, 529 MACE, 310 all cause deaths, 193 CV deaths, and 157 hHF events occurred. Baseline NT-proBNP was strongly prognostic (adjusted HR per 1 integer unit 1.63 for MACE, 1.85 for ACM, 2.17 for CV death, and 2.17 for hHF; all P < .001). Baseline cTnI was also prognostic with a nonlinear pattern, with risk rising mainly above the median. Per SD rise in NT-proBNP over 1 year predicted later MACE (HR 1.85) and CV death (HR 2.81; both P < .001). Baseline NT-proBNP didn't modify treatment effects. Baseline cTnI didn't modify EQW treatment effect on MACE but lower rates of CV deaths and hHF with EQW were observed at higher cTnI concentrations. NT-proBNP and cTnI were strong prognostic markers of adverse outcomes in patients with type 2 diabetes and their 1-year increases signaled higher subsequent risk. Baseline cTnI may mark heterogeneity of EQW response, but mortality interactions are hypothesis generating and require confirmation.

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.