dc.contributor.author | Gálvez Fernandez, Marta | |
dc.contributor.author | Rodríguez Hernández, Zulema | |
dc.contributor.author | Grau Pérez, María | |
dc.contributor.author | Chaves, Felipe Javier | |
dc.contributor.author | García García, Ana Bárbara | |
dc.contributor.author | Amigo, Nuria | |
dc.contributor.author | Monleon, Daniel | |
dc.contributor.author | García Barrera, Tamara | |
dc.contributor.author | Gómez Ariza, José L. | |
dc.contributor.author | Briongos Figuero, Laisa Socorro | |
dc.contributor.author | Pérez Castrillon, José Luis | |
dc.contributor.author | Redón Mas, Josep | |
dc.contributor.author | Téllez Plaza, Maria | |
dc.contributor.author | Martín Escudero, Juan Carlos | |
dc.date.accessioned | 2024-10-28T12:44:28Z | |
dc.date.available | 2024-10-28T12:44:28Z | |
dc.date.issued | 2023 | |
dc.identifier.citation | Free Radical Biology and Medicine, 2023, vol. 194, p. 52-61. | es |
dc.identifier.issn | 0891-5849 | es |
dc.identifier.uri | https://uvadoc.uva.es/handle/10324/70983 | |
dc.description | Producción Científica | |
dc.description.abstract | Background:
The potential joint influence of metabolites on bone fragility has been rarely evaluated. We assessed the association of plasma metabolic patterns with bone fragility endpoints (primarily, incident osteoporosis-related bone fractures, and, secondarily, bone mineral density BMD) in the Hortega Study participants. Redox balance plays a key role in bone metabolism. We also assessed differential associations in participant subgroups by redox-related metal exposure levels and candidate genetic variants.
Material and methods:
In 467 participants older than 50 years from the Hortega Study, a representative sample from a region in Spain, we estimated metabolic principal components (mPC) for 54 plasma metabolites from NMR-spectrometry. Metals biomarkers were measured in plasma by AAS and in urine by HPLC-ICPMS. Redox-related SNPs (N = 341) were measured by oligo-ligation assay.
Results:
The prospective association with incident bone fractures was inverse for mPC1 (non-essential and essential amino acids, including branched-chain, and bacterial co-metabolites, including isobutyrate, trimethylamines and phenylpropionate, versus fatty acids and VLDL) and mPC4 (HDL), but positive for mPC2 (essential amino acids, including aromatic, and bacterial co-metabolites, including isopropanol and methanol). Findings from BMD models were consistent. Participants with decreased selenium and increased antimony, arsenic and, suggestively, cadmium exposures showed higher mPC2-associated bone fractures risk. Genetic variants annotated to 19 genes, with the strongest evidence for NCF4, NOX4 and XDH, showed differential metabolic-related bone fractures risk.
Conclusions:
Metabolic patterns reflecting amino acids, microbiota co-metabolism and lipid metabolism were associated with bone fragility endpoints. Carriers of redox-related variants may benefit from metabolic interventions to prevent the consequences of bone fragility depending on their antimony, arsenic, selenium, and, possibly, cadmium, exposure levels. | es |
dc.format.mimetype | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Elsevier | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.subject.classification | Metabolomics | es |
dc.subject.classification | Bone mineral density | |
dc.subject.classification | Osteoporosis-related bone fractures | |
dc.subject.classification | Candidate genes | |
dc.subject.classification | Metals | |
dc.subject.classification | Redox | |
dc.title | Metabolomic patterns, redox-related genes and metals, and bone fragility endpoints in the Hortega Study | es |
dc.type | info:eu-repo/semantics/article | es |
dc.identifier.doi | 10.1016/j.freeradbiomed.2022.11.007 | es |
dc.relation.publisherversion | https://www.sciencedirect.com/science/article/pii/S0891584922009698 | |
dc.identifier.publicationfirstpage | 52 | es |
dc.identifier.publicationlastpage | 61 | es |
dc.identifier.publicationtitle | Free Radical Biology and Medicine | es |
dc.identifier.publicationvolume | 194 | es |
dc.peerreviewed | SI | es |
dc.description.project | The work was funded by the´o State Research Agency at the Ministerio de Ciencia Innovaci´on y Universidades of Spain (PID2019- 108973RB-C21, PID2019-108973RB-C22 and PCIN-2017-117); the Generalitat Valenciana of Spain (IDIFEDER/2021/072, GRUPOS 03/ 101, PROMETEO/2009/029, ACOMP/2013/039, IDIFEDER/2021/072 and GRISOLIAP/2021/119); the EU Joint Programming Initiative Healthy Diet Healthy Life (HDHL) GUTMOM (INTIMIC-085); the Strategic Action for Research in Health sciences [CP12/03080, PI15/00071, PI10/0082, PI13/01848, PI14/00874, PI16/01402, PI17/00544 and PI11/00726]; CIBER Fisiopatología Obesidad y Nutrici´on (CIBEROBN) (CIBER-02-08-2009, CB06/03 and CB12/03/30016); the Castilla-Leon Government (GRS/279/A/08) and European Network of Excellence Ingenious Hypercare (EPSS- 037093) from the European Commission. The Strategic Action for Research in Health sciences and CIBEROBN are initiatives from Carlos III Health Institute Madrid and co-funded with European Funds for Regional Development (FEDER). M.G-P received the support of a fellowship from “la Caixa” Foundation (ID 100010434, fellowship code LCF/BQ/IN18/11660001). | |
dc.type.hasVersion | info:eu-repo/semantics/publishedVersion | es |