PubMed

Nutrients. 2025 Apr 7;17(7):1289. doi: 10.3390/nu17071289.ABSTRACTBACKGROUND: Salt sensitivity of blood pressure (SSBP) is an important risk factor for essential hypertension and cardiovascular diseases, and its metabolic mechanisms remain poorly understood. This study aimed to identify SSBP-associated metabolic biomarkers and investigate their potential mediating role in the SSBP-hypertension pathophysiology.METHODS: Based on the Systematic Epidemiological Study of Salt Sensitivity (EpiSS) conducted in 2014-2016, we performed a case-control study involving 54 matched pairs of participants classified as salt-sensitive or salt-resistant with targeted metabolomics detected. Multivariable logistic regression analyses were conducted to assess the metabolites associations with SSBP and hypertension. The diagnostic performance of the model was evaluated using the receiver operating characteristic curve (ROC) analysis yielded an area under the curve (AUC) value, sensitivity, and specificity. Furthermore, the potential mediating effects of targeted metabolites on the relationship between SSBP and essential hypertension were explored.RESULTS: Three metabolites demonstrated significant SSBP associations: L-Glutamine (OR = 0.998; 95% CI: 0.997, 0.999), PC (16:1/14:0) (OR = 1.039; 95% CI: 1.003, 1.077), and ChE (22:4) (OR = 1.115; 95% CI: 1.002, 1.240). Among them, L-Glutamine demonstrated the highest diagnostic efficiency for SSBP (AUC = 0.766; 95% CI: 0.677, 0.855). The combined model of the three metabolites slightly improved diagnostic efficiency (AUC = 0.788; 95% CI: 0.703, 0.874). L-Glutamine and Cer (d18:0/24:1) were identified as potential protective factors against essential hypertension (p < 0.05). Mediation analyses further indicated that L-Glutamine partially mediated the relationship between SSBP and essential hypertension, demonstrating a suppressive effect.CONCLUSIONS: This study identified L-Glutamine as both a diagnostic biomarker for SSBP and a metabolic modulator attenuating hypertension risk, providing insights for early SSBP screening and the pathways governing SSBP progression to overt hypertension.PMID:40219046 | DOI:10.3390/nu17071289

Nutrients. 2025 Mar 26;17(7):1146. doi: 10.3390/nu17071146.ABSTRACTBackground: Dietary fibre plays a crucial role in metabolic regulation, inflammation, and microbiome composition. However, its impact on systemic and oral health, particularly in periodontitis, remains unclear. This study investigated the effects of high- and low-fibre diets on body composition, glycaemic control, inflammation, microbiome, and metabolome in a murine model of experimental periodontitis. Methods: Thirty-six male C57BL/6 mice were randomised to a high-fibre (40% fibre) or low-fibre (5% fibre) diet for eight weeks. Body weight, fat mass, lean mass, fasting blood glucose, serum inflammatory markers, alveolar bone loss, and root length were assessed. Oral and faecal microbiome composition was analysed using 16S rRNA sequencing. Metabolomic and short-chain fatty acid (SCFA) profiling was conducted using liquid chromatography-mass spectrometry (LC-MS). Results: Mice on the high-fibre diet exhibited significantly lower body weight (p < 0.0001), fat mass (p = 0.0007), and lean mass (p < 0.0001) compared to the low-fibre group. Fasting blood glucose levels were significantly lower in the high-fibre group (p = 0.0013). TNF-α and IFN-γ levels were significantly elevated in the low-fibre group (p < 0.0001), suggesting a heightened pro-inflammatory state. While alveolar bone loss and root length did not differ significantly, microbiome analysis revealed distinct bacterial compositions (PERMANOVA, p < 0.05), with fibre-fermenting taxa enriched in high-fibre-fed mice. Metabolomic analysis identified 19 significantly altered metabolites, indicating dietary adaptations. Conclusions: A high-fibre diet improves glycaemic control, reduces systemic inflammation, and alters microbial and metabolic profiles in experimental periodontitis. These findings highlight dietary fibre's role in modulating metabolic and inflammatory pathways relevant to periodontal and systemic diseases.PMID:40218904 | DOI:10.3390/nu17071146

Nutrients. 2025 Mar 22;17(7):1113. doi: 10.3390/nu17071113.ABSTRACTBackground/Objectives: Melanoma is an aggressive skin cancer with intratumor metabolic heterogeneity, which drives its progression and therapy resistance. Natural anthraquinones, such as emodin and aloe-emodin, exhibit anti-cancer properties, but their effects on metabolic plasticity remain unclear. This study evaluated their impact on proliferation and metabolic pathways in heterogenous melanoma human cell lines. Methods: COLO 800, COLO 794, and A375 melanoma cell lines representing distinct metabolic phenotypes were analyzed. Targeted and untargeted metabolomics analyses integrated with Seahorse assays were performed to assess the effects of emodin and aloe-emodin on cell proliferation, mitochondrial function, and redox homeostasis. Glucose tracing using [U-13C6] glucose and metabolic flux analysis (MFA) were carried out to evaluate the glycolysis and TCA cycle dynamics. Results: Emodin and aloe-emodin inhibited proliferation by disrupting glycolysis, oxidative phosphorylation, and energy production across all cell lines. Both compounds impaired glucose metabolism, reduced TCA cycle intermediates, and induced mitochondrial ROS accumulation, causing oxidative stress and redox imbalance. Despite intrinsic metabolic differences, COLO 800 and COLO 794 upregulated antioxidant defenses; A375 enhanced one-carbon metabolism and amino acid pathways to maintain redox balance and nucleotide biosynthesis. Conclusions: Emodin and aloe-emodin can disrupt the metabolic plasticity of melanoma cells by impairing glycolysis, mitochondrial function, and redox homeostasis. Their ability to target metabolic vulnerabilities across diverse phenotypes highlights their therapeutic potential for overcoming resistance mechanisms and advancing melanoma treatment strategies.PMID:40218871 | DOI:10.3390/nu17071113

Animals (Basel). 2025 Apr 4;15(7):1053. doi: 10.3390/ani15071053.ABSTRACTIn order to optimize diets for Bengal tiger cubs and improve their health condition and survival rates, we conducted microbiota and metabolomics analyses on fecal samples from Bengal tiger cubs fed goat and dog milk replacer formulae. The results showed that there were significant differences in fecal microorganisms and metabolites between the two groups. At the phylum level, the major components of the microbial composition in the feces of cubs were Firmicutes, Actinobacteriota, Proteobacteria, Bacteroidota and Fusobacteriota. In addition, the abundance of gut microbiota varied significantly between the two groups of tiger cubs. The fecal microbiota of the tiger cubs fed dog milk replacer powder exhibited an increase in probiotic bacteria (Anaerostipes and Clostridium_scindens) (p < 0.05), and the microbial community tended to be more balanced. Metabolomics data further elucidated that feeding different milk formulae significantly affected the fecal metabolites and metabolic pathways in the Bengal tiger cubs. In the dog milk replacer powder group, 76 metabolites were up-regulated (p < 0.05), and 278 metabolites were down-regulated (p < 0.05), particularly affecting the metabolism of vitamin D3, vitamin B5, isoleucine, valine, phenylalanine and oleic acid. At the same time, 19 metabolic pathways were affected (p < 0.05), including the amino acid metabolism, lipid metabolism and nucleotide metabolism pathways. In conclusion, this study confirms that milk formula composition affects the gut microbiota and metabolism of Bengal tiger cubs. These findings may provide new insights into how different milk powder formulae and dietary strategies influence the regulation of gut microbiota and overall health in Bengal tiger cubs.PMID:40218446 | DOI:10.3390/ani15071053

Animals (Basel). 2025 Mar 22;15(7):912. doi: 10.3390/ani15070912.ABSTRACTEgg production is a complex biological process closely linked to ovarian development and metabolic adaptation in laying hens. As the core reproductive organ, the ovary undergoes significant changes during different egg-laying stages. This study employed untargeted metabolomics to analyze metabolites in serum and ovarian tissues of hens at 20W and 30W. The results revealed that metabolic reprogramming in ovarian tissues was more pronounced than in serum. Shared metabolites between serum and ovarian tissues demonstrated coordinated interactions between systemic and local metabolic networks. The synthesis of prostaglandin E1 during lipid metabolism was identified as a key driver of ovulation and hormone production. Extracellular matrix remodeling and polyamine metabolism, particularly spermidine/spermine, enhanced cell adhesion and antioxidant capacity during ovarian development. These findings provide new insights into follicular development, ovulation regulation, and steroid hormone biosynthesis, while suggesting potential metabolic targets to improve poultry reproductive efficiency.PMID:40218306 | DOI:10.3390/ani15070912

J Clin Med. 2025 Apr 3;14(7):2459. doi: 10.3390/jcm14072459.ABSTRACTKeratoconus (KC) is a progressive ocular disorder marked by structural and functional alterations of the cornea, leading to significant visual impairment. Recent studies indicate that these corneal changes are linked to molecular and cellular mechanisms that disrupt and degrade the extracellular matrix. This degradation is influenced by proteinases that contribute to a loss of homeostasis and an imbalance in the antioxidant/oxidative state within the cornea, fostering oxidative stress, inflammation, and apoptosis. Although these biological processes have been identified primarily through molecular biology research, omics technologies have significantly advanced our understanding of the physiological and pathological phenomena associated with KC. Omics studies encompassing genomics, transcriptomics, proteomics, epigenomics, and metabolomics, have emerged as critical tools in elucidating the complex biological landscape of various diseases, including ocular conditions. The integrative application of these studies has demonstrated their potential in personalizing medicine across diverse fields such as oncology, neurology, and ophthalmology. This review aims to describe findings from omics research applied to keratoconus, highlighting the genomic, transcriptomic, proteomic, epigenomic, and metabolomic aspects derived from ocular and other biological samples. Notably, the molecular insights gained from these studies hold promise for identifying biomarkers of keratoconus, which could enhance diagnostic accuracy and therapeutic strategies. The exploration of these biomarkers may facilitate improved management and treatment options for patients, contributing to personalized care in keratoconus management.PMID:40217908 | DOI:10.3390/jcm14072459

J Clin Med. 2025 Apr 2;14(7):2432. doi: 10.3390/jcm14072432.ABSTRACTAntiseizure medication (ASM) induced metabolic syndrome (AIMetS) is a common adverse drug reaction (ADR) of pharmacotherapy for epilepsy and psychiatric disorders. However, the sensitivity and specificity of blood biomarkers may be insufficient due to the influence of combined pathology, concomitant diseases, and the peculiarities of the metabolism of ASMs in patients with epilepsy. Methods: The presented results of experimental and clinical studies of microRNAs (miRs) as epigenetic biomarkers of MetS and AIMetS, which were entered into the different databases, were analyzed for the last decade (2014-2024). Results: A systematic review demonstrated that miRs can act as promising epigenetic biomarkers of key AIMetS domains. However, the results of the review demonstrated the variable role of various miRs and their paralogs in the pathogenesis of AIMetS. Therefore, as part of this study, an miRs signature was proposed that allows us to assess the risk of developing and the severity of AIMetS as low risk, medium risk, and high risk. Conclusions: The mechanisms of development and biomarkers of AIMetS are an actual problem of epileptology, which is still far from being resolved. The development of panels (signatures) of epigenetic biomarkers of this widespread ADR may help to increase the safety of pharmacotherapy of epilepsy. However, to increase the sensitivity and specificity of circulating miRs in the blood as biomarkers of AIMetS, it is necessary to conduct "bridge" studies in order to replicate the results of preclinical and clinical studies into real clinical practice.PMID:40217882 | DOI:10.3390/jcm14072432

J Clin Med. 2025 Mar 28;14(7):2339. doi: 10.3390/jcm14072339.ABSTRACTEndometriosis is a complex and multifaceted gynecological disorder characterized by the abnormal growth and presence of endometrial-like tissue outside the confines of the uterine cavity. It can lead to a wide range of distressing symptoms, including chronic pelvic pain, heavy and/or irregular menstrual bleeding, and significant challenges with fertility. While the association between endometriosis and infertility is well recognized, the precise mechanisms through which the disease affects oocyte and embryo quality remain controversial. Studies that utilized transcriptomic, metabolomic, and ultrastructural analyses indicated dysregulated energy metabolism, oxidative stress, mitochondrial dysfunction, and inflammatory alterations in the ovarian microenvironment. The impact of endometriosis on fertilization, embryo development, and implantation remains debated, with conflicting findings across different study designs. Some investigations reported impaired oocyte morphology, reduced fertilization rates, and poorer embryo quality, while others suggested that endometriosis does not significantly affect ART outcomes when confounding factors are controlled. Recent studies highlight the importance of distinguishing the disease severity, lesion location, and prior surgical interventions when assessing reproductive outcomes. The need for standardized methodologies in evaluating oocyte and embryo quality, alongside personalized treatment approaches, is emphasized. Further research is warranted to elucidate the precise molecular mechanisms underlying these effects and to develop targeted therapeutic strategies aimed at improving ART success in women with endometriosis. This narrative review provides a thorough examination of the previous research on the impact of endometriosis on oocyte and embryo quality, highlighting both the known mechanisms and the areas that require further investigation. This will help to guide future research and clinical management strategies to improve reproductive outcomes for women with endometriosis.PMID:40217789 | DOI:10.3390/jcm14072339

Biol Direct. 2025 Apr 11;20(1):51. doi: 10.1186/s13062-025-00635-w.ABSTRACTMutations in the tumour suppressor protein p53 are present in 70% of human pancreatic ductal adenocarcinomas (PDAC), subsequently to highly common activation mutation of the oncogene KRAS. These p53 mutations generate stable expression of mutant proteins, such as p53R175H and p53R273H, which do not retain p53 wild type function. In this study, we investigated the impact of two specific p53 mutant variants on lipid metabolism of pancreatic cancer. Lipids critically participate to tumorigenesis with to their roles in membrane biosynthesis, energy storage and production of signalling molecules. Using cell lines derived from mouse models of PDAC generated by knock-in p53 alleles carrying point mutations at codons R172H and R270H (equivalent to R175H and R273H in humans), we found that silencing p53R172H and p53R270H in pancreatic cancer cells significantly alters lipid metabolism, with patterns of common and variant specific changes. Specifically, loss of p53R172H in these cells reduces lipid storage. Additionally, silencing either p53R172H or p53R270H individually leads to marked increases in lysophospholipid levels. These findings offer new insights into the lipidome reprogramming induced by the loss of mutant p53 and underscore changes in lipid storage as a potential key molecular mechanism in PDAC pathogenesis.PMID:40217553 | DOI:10.1186/s13062-025-00635-w

BMC Gastroenterol. 2025 Apr 11;25(1):247. doi: 10.1186/s12876-025-03858-3.ABSTRACTBACKGROUND: Plasma lipid homeostasis is pivotal in maintaining intestinal health. Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn's disease (CD) as distinct subtypes, manifests unique metabolic signatures. However, the specific roles of lipids in the pathogenesis and therapeutic targeting of IBD remain inadequately explored. This study aims to delineate the genetic influences of plasma lipids on IBD risk.METHODS: We obtained genome-wide association study (GWAS) summary statistics of lipidomes and IBD (including UC and CD) from published studies to perform two-sample Mendelian randomization (MR) analyses. Outliers were removed using radial MR, followed by the application of the inverse-variance weighted (IVW) method to assess causal relationships. Sensitivity analyses were also conducted to validate the robustness of the primary results of the MR analyses. Additionally, reverse MR analyses were performed to evaluate the potential for reverse causality.RESULTS: The MR analysis identified fourteen lipid species significantly associated with IBD, four with UC, and ten with CD. Phosphatidylcholine (PC; P < 0 .05) and lysophosphatidylcholine (OR = 0.83, P < 0.001) were instrumental in UC, while in CD, alongside these, cholesterol ester (OR = 0.86, P < 0.001), diacylglycerol (OR = 1.21, P = 0.004), and lysophosphatidylethanolamine (OR = 1.30, P < 0.001) also demonstrated causal links. Reverse MR analysis revealed no significant associations between IBDs and 179 lipid species.CONCLUSION: This bidirectional MR study has uncovered genetic evidence of a causal relationship between lipidome and IBD, identifying potential therapeutic targets for IBD treatment. The findings suggest that elevated partial phosphatidylcholine, lysophosphatidylcholine, and cholesterol ester levels could reduce the risk of IBD, indicating a potential protective role for these lipid molecules. This study also underscores the critical role of lipidome variability in advancing our understanding of IBD's pathogenic processes and in developing targeted therapies.PMID:40217472 | DOI:10.1186/s12876-025-03858-3

Chin Med. 2025 Apr 11;20(1):48. doi: 10.1186/s13020-025-01094-1.ABSTRACTBACKGROUND: The popularity of herbal formulas is increasing worldwide. Nevertheless, the effective compound is challenging to identify due to its intricate composition and multiple targets.METHODS: An integration machine learning-assisted approach was established, whereby the particular action mechanism and direct target were obtained through the correlation of compounds, targets, and metabolites. The association between a compound and an action pathway was selected from the shortest path of the "compound-target-pathway-disease" network, which was analyzed using the Floyd-Warshall algorithm. Subsequently, an investigation was conducted into the relationship between metabolites and action pathways, as well as targets, through the analysis of serum metabolomic profiling and the selection of metabolite biomarkers by random forest. In order to accurately identify the direct acting target as well as the most effective compound, the relationship between the compounds and their targets was investigated using a feature-based prediction model conducted by AdaBoost. The binding mode of the effective compound and the direct-acting target was verified by molecular docking, dynamics simulations, and western blotting. In this study, Baiji Wuweizi Granule (BWG) was employed to elucidate the effective compound against alcoholic liver injury (ALD).RESULTS: BWG exerted an influence on the serum metabolomic, resulting in the identification of seven potential biomarkers. Furthermore, six effective compounds and the PI3K-AKT signalling pathway were identified through a co-analysis with the shortest path from compound to ALD in the "compound-target-pathway-disease" network. It was postulated that the effective compounds would bind with key targets from the PI3K-AKT signaling pathway, as indicated by the prediction model of compound-target interaction (R2 > 0.95). The dominant bonding type for the effective compounds and key targets was hydrogen bond. These results indicated that AKT1 was the notable target for BWG, and that 2,3,4,7-tetramethoxyphenanthrene was the marker compound for BWG against ALD. The present study provides evidence that the protective effect of BWG on ALD can be mediated by the PI3K-AKT signaling pathway.CONCLUSIONS: Our findings demonstrate the value of a machine learning-assisted approach in identifying the key compound, target and pathway that underpin the efficacy of an herbal formula. This provides a foundation for future clinical and fundamental research.PMID:40217538 | DOI:10.1186/s13020-025-01094-1

Nat Med. 2025 Apr 11. doi: 10.1038/s41591-025-03608-8. Online ahead of print.ABSTRACTThe European Union-sponsored ONCOBIOME network has spurred an international effort to identify and validate relevant gut microbiota-related biomarkers in oncology, generating a unique and publicly available microbiome resource. ONCOBIOME explores the effects of the microbiota on gut permeability and metabolism as well as on antimicrobial and antitumor immune responses. Methods for the diagnosis of gut dysbiosis have been developed based on oncomicrobiome signatures associated with the diagnosis, prognosis and treatment responses in patients with cancer. The mechanisms explaining how dysbiosis compromises natural or therapy-induced immunosurveillance have been explored. Through its integrative approach of leveraging multiple cohorts across populations, cancer types and stages, ONCOBIOME has laid the theoretical and practical foundations for the recognition of microbiota alterations as a hallmark of cancer. ONCOBIOME has launched microbiota-centered interventions and lobbies in favor of official guidelines for avoiding diet-induced or iatrogenic (for example, antibiotic- or proton pump inhibitor-induced) dysbiosis. Here, we review the key advances of the ONCOBIOME network and discuss the progress toward translating these into oncology clinical practice.PMID:40217075 | DOI:10.1038/s41591-025-03608-8

Sci Rep. 2025 Apr 11;15(1):12494. doi: 10.1038/s41598-025-97312-9.ABSTRACTMetabolic associated fatty liver disease (MAFLD) represents a significant public health concern. Previous studies have shown that ACT001 has therapeutic effects on MAFLD. This study investigated the potential mechanisms by which ACT001 may treat MAFLD through an integrated approach of transcriptomics and metabolomics. MAFLD model induced by high-fat diet was established, and ACT001 was given by gavage. Histological analysis was performed, and liver enzyme and lipid levels were measured. Transcriptomic analysis was performed to identify differentially expressed genes, while metabolomic analysis was used to detect differential metabolites. Pathways enriched by genes and metabolites affected by ACT001 were also identified. The differentially expressed genes were confirmed through RT-qPCR. ACT001 reduced the levels of liver enzymes and lipids, and alleviated pathological damage such as hepatic steatosis. The integration of transcriptomic and metabolomic analyses indicated that ACT001 may alleviate high-fat diet-induced MAFLD by regulating the linoleic acid and glutathione metabolic pathways. The validation of five differentially expressed genes using RT-qPCR yielded results that were consistent with the transcriptomics data. ACT001 may exert a therapeutic effect in MAFLD mice by modulating glutathione metabolism and linoleic acid metabolism. It has the potential to be a promising treatment for MAFLD.PMID:40216908 | DOI:10.1038/s41598-025-97312-9

Sci Rep. 2025 Apr 11;15(1):12533. doi: 10.1038/s41598-025-96386-9.ABSTRACTHypoxia is a contributing factor for the morbidity and mortality in patients with obstructive sleep apnea (OSA). We aimed at identifying the percentage of sleep time with oxyhemoglobin desaturation below 90% (Tc90%) breakpoint from which the most significant changes occur in systemic metabolome of patients with OSA. In a prospective observational study on patients with polysomnography-confirmed symptomatic OSA, profiles of 186 metabolites including amino acids, biogenic amines, acylcarnitines (AC), lysophosphatidylcholines, phosphatidylcholines (PC) and sphingomyelins (SM) were analyzed with liquid chromatography-mass-spectrometry in peripheral blood, obtained at 3 time points that covered patients' night sleep. Comparisons of rank-transformed data with general linear model for repeated measures after dichotomizing the study group at different Tc90% levels were applied to define the best cut-off, hypoxic metabolic threshold (HMT), based on Cohen's f. Fifty-one subjects were recruited with their median Tc90% of 2.1. The mean Cohen's f over the metabolites was highest (0.165) at a Tc90% of 1.8 representing the HMT. Of the different classes of metabolites, the Cohen's f value at HMT was highest for SM (0.322). Compared to patients with Tc90% < HMT, concentrations of 2 PC, 1 AC and 7 SM were significantly higher in patients with Tc90% ≥HMT. The HMT for patients with OSA described in this report for the first time is located at a Tc90% level of 1.8 with SM levels contributing most to the size of this threshold.PMID:40216838 | DOI:10.1038/s41598-025-96386-9

Sci Rep. 2025 Apr 11;15(1):12410. doi: 10.1038/s41598-025-89600-1.ABSTRACTHashimoto's thyroiditis (HT), one of the most common autoimmune diseases and the leading cause of hypothyroidism, is linked to metabolic and cellular dysfunctions that contribute to disease aetiopathogenesis. This case-control study aimed to identify potent metabolic biomarkers of HT employing machine learning techniques. 62 euthyroid patients with HT and 58 healthy individuals were included from the metabolic biomarkers in Hashimoto's thyroiditis and psoriasis (METHAP) clinical trial. Quantification of 73 metabolites was performed using gas-chromatography/mass spectrometry in plasma and urine samples of fasted participants. Changes in the tricarboxylic acid cycle, carbohydrate, neurotransmitter, microbiome and lipid metabolism were identified in the HT group. Ordinary least squares and beta regression modeling associated the presence of HT with methylmalonic acid, 4-hydroxyphenylpyruvic acid, palmitic acid, palmitoleic acid, myristoleic acid and total saturated fatty acids, adjusting for confounders. Artificial neural network analysis had good predictive accuracy with an AUC of 0.8, while debiased sparse partial correlation network analysis identified metabolite-metabolite interactions distinct for HT. These findings provide insights into novel biomarkers associated with HT, and we discuss their biological relevance and clinical significance. Hashimoto's thyroiditis is associated with mitochondrial dysfunction, micronutrient decreased bioavailability, microbiome imbalances, and carbohydrate and fatty acids dysfunctional metabolism.PMID:40216810 | DOI:10.1038/s41598-025-89600-1

NPJ Aging. 2025 Apr 12;11(1):26. doi: 10.1038/s41514-025-00218-z.ABSTRACTIncreasing evidence suggests that frailty results from a complex age-associated metabolic decline. Here, we investigated the serum metabolomic profile of a well-characterized cohort of elderly subjects encompassing the whole fit-to-frail continuum. Enrichment analyses revealed a complex dysregulation of amino acids and energy metabolism in both pre-frail and frail participants. Remarkably, upregulated betaine levels emerged as a specific biochemical signature of pre-frail females, holding promise for the development of novel targeted interventions.PMID:40216769 | DOI:10.1038/s41514-025-00218-z

Metabolomics. 2025 Apr 11;21(3):51. doi: 10.1007/s11306-025-02251-1.NO ABSTRACTPMID:40216608 | DOI:10.1007/s11306-025-02251-1

Angew Chem Int Ed Engl. 2025 Apr 11:e202502028. doi: 10.1002/anie.202502028. Online ahead of print.ABSTRACTInnovations in spatial omics technologies applied to human tissues have led to breakthrough discoveries in various diseases, including cancer. Two of these approaches - spatial transcriptomics and spatial metabolomics - have blossomed independently, fueled by technologies such as spatial transcriptomics (ST) and mass spectrometry imaging (MSI). While powerful, these technologies only offer insights into the spatial distributions of restricted classes of molecules and have not yet been integrated to provide more holistic insights into biological questions. These techniques can be performed on adjacent serial sections from the same sample, but section-to-section variability can convolute data integration. We present a novel method combining desorption electrospray ionization mass spectrometry imaging (DESI-MSI) spatial metabolomics and Visium spatial transcriptomics on the same tissue sections. We show that RNA quality is maintained after performing DESI-MSI on a tissue and that ST data is unperturbed following DESI-MSI. We demonstrate this workflow on human breast and lung cancer tissues and identify novel correlations between metabolites and RNA transcripts in cancer specific regions.PMID:40216587 | DOI:10.1002/anie.202502028

Nutr Metab Cardiovasc Dis. 2025 Apr 4:104031. doi: 10.1016/j.numecd.2025.104031. Online ahead of print.ABSTRACTBACKGROUND AND AIMS: To explore the metabolomic profiles of different body shapes, their potential similarities and differences, and their associations with the risks of incident cardiovascular diseases.METHODS AND RESULTS: Plasma metabolite, body mass index (BMI), and waist-to-height ratio (WHtR) data were available in 7471 Chinese adults. We categorized body shapes into four groups by combining BMI (low: <24 kg/m2, high: ≥24 kg/m2) with WHtR (low: <0.5, high: ≥0.5). We used linear regression and enrichment analysis to characterize metabolomic profiles and elastic-net regression to construct metabolite scores for body shapes. In nested case-control studies, we explored the associations of metabolite scores with the risks of coronary heart disease, acute coronary syndrome (ACS), and stroke, including 1621, 657, and 1289 case-control pairs, respectively. Compared with low BMI and low WHtR, four shared (e.g. arginine and proline metabolism) and eight specific (e.g. glutathione metabolism) metabolite sets were identified for the other three body shapes. Metabolite scores for low BMI and high WHtR, and high BMI and low WHtR were associated with increased and decreased risks of ACS, respectively [odd ratios (95 % confidence intervals): 1.28 (1.14, 1.45) and 0.81 (0.72, 0.91)]. The metabolite score for high BMI and high WHtR was associated with increased risks of ACS, total and ischemic stroke [odd ratios (95 % confidence intervals): 1.21 (1.07, 1.37), 1.10 (1.01, 1.21), and 1.15 (1.04, 1.28)].CONCLUSIONS: This study unveiled metabolomic profiles of different body shapes, the underlying similarities and differences, and their associations with incident cardiovascular diseases.PMID:40216564 | DOI:10.1016/j.numecd.2025.104031

J Appl Microbiol. 2025 Apr 11:lxaf089. doi: 10.1093/jambio/lxaf089. Online ahead of print.ABSTRACTAIMS: Phenoxyethanol is a broad-spectrum antimicrobial agent widely used in cosmetic formulations. However, its antibacterial effects on different skin bacteria, particularly the predominant Cutibacterium acnes and its various phylotypes, remain unclear. The objective of this study was to examine the antimicrobial effects of phenoxyethanol on C. acnes and explore the mechanism.METHODS AND RESULTS: Phenoxyethanol exhibited strong antimicrobial effects against both C. acnes ATCC6919 (phylotype IA1) and CCSM0331 (phylotype II), achieving a minimum inhibitory concentration (MIC) of 0.5% (v/v). Sub-MIC concentrations showed a stronger inhibitory effect on CCSM0331. RNA-seq and metabolomic analyses revealed that phenoxyethanol disrupted cell membrane integrity and influenced essential metabolic pathways, such as energy metabolism, amino acid metabolism, and pyrimidine metabolism. Additionally, glycolysis and the Wood-Werkman cycle were inhibited in CCSM0331 but enhanced in ATCC6919. The expression of genes involved in porphyrin metabolism, associated with inflammation, was significantly reduced.CONCLUSIONS: Phenoxyethanol exhibits the antimicrobial activity against C. acnes, with differential effects on phylotypes, targeting critical metabolic pathways and cellular processes. These findings indicate its potential for acne treatment.PMID:40216407 | DOI:10.1093/jambio/lxaf089