<HashMap><database>MetaboLights</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Tabular>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13125/m_MTBLS13125_LC-MS_positive_reverse-phase_metabolite_profiling_v2_maf.tsv</Tabular><Tabular>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13125/m_MTBLS13125_LC-MS_negative_reverse-phase_metabolite_profiling_v2_maf.tsv</Tabular><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13125/i_Investigation.txt</Txt><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13125/a_MTBLS13125_LC-MS_negative_reverse-phase_metabolite_profiling.txt</Txt><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13125/a_MTBLS13125_LC-MS_positive_reverse-phase_metabolite_profiling.txt</Txt><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13125/s_MTBLS13125.txt</Txt></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><ftp_download_link>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13125</ftp_download_link><metabolite_identification_protocol>&lt;p>Metabolite identification was performed in Compound Discoverer™ by matching fragmentation spectra (MS/MS) and accurate mass (MS1) against multiple databases. These included the in-house mzVault library, public online libraries (mzCloud, HMDB, KEGG, LIPID MAPS, MoNA), and the NIST_2020_MSMS spectral library. Identification criteria included a precursor mass tolerance of 15 ppm and an MS2 match factor threshold of 50.&lt;/p></metabolite_identification_protocol><repository>MetaboLights</repository><study_status>Public</study_status><ptm_modification></ptm_modification><instrument_platform>Liquid Chromatography MS - negative - reverse phase</instrument_platform><instrument_platform>Liquid Chromatography MS - positive - reverse phase</instrument_platform><chromatography_protocol>&lt;p>Chromatographic separation was performed on an ACQUITY UPLC HSS T3 column (100Å, 1.8 µm, 2.1 mm × 100 mm). The mobile phase consisted of 0.1% formic acid in water (Phase A) and acetonitrile containing 0.1% formic acid (Phase B). Separation was achieved using a gradient elution at a flow rate of 0.4 mL/min. The column temperature was maintained at 40°C and the injection volume was 2 µL.&lt;/p></chromatography_protocol><publication>Gut commensal Odoribacter splanchnicus alleviates hyperlipidemic periodontitis via the β-GPA-TLR4 axis.</publication><submitter_name>Jing Xu</submitter_name><submitter_affiliation>Jilin University Stomatological Hospital</submitter_affiliation><organism_part>cecal contents</organism_part><technology_type>mass spectrometry assay</technology_type><disease></disease><extraction_protocol>&lt;p>Approximately 20-50 mg of intestinal content was weighed into a 2 mL centrifuge tube. Metabolites were extracted by adding 500 µL of pre-cooled methanol containing a 5 ppm internal standard (2-chlorophenylalanine), followed by homogenization using a high-throughput grinder (55 Hz, 60 s). The mixture was then ultrasonicated for 10 min, frozen at -20°C for 30 min, and centrifuged at 12,000 rpm for 10 min at 4°C. The resulting supernatant was collected for analysis.&lt;/p></extraction_protocol><organism>Mus musculus</organism><full_dataset_link>https://www.ebi.ac.uk/metabolights/MTBLS13125</full_dataset_link><author>Di Wang. School of Life Sciences, Jilin University. jluwangdi@jlu.edu.cn.</author><author>Min Hu. Department of Orthodontics, Hospital of Stomatology, Jilin University. humin@jlu.edu.cn.</author><author>Jing Xu. The Bethune Hospital of Stomatology, Jilin University. xujing23@mails.jlu.edu.cn.</author><data_transformation_protocol>&lt;p>The raw .raw files were imported into Compound Discoverer™ software (v3.3). The workflow included peak detection, alignment, and correction using the software's algorithms. Peaks not detected in over 50% of QC samples were filtered. Missing values for remaining peaks were imputed using the Fill Gaps algorithm, and the data was then normalized by the total peak area (Sum normalization) to ensure comparability across samples.&lt;/p></data_transformation_protocol><study_factor>Disease</study_factor><submitter_email>huzz22@mails.jlu.edu.cn</submitter_email><sample_collection_protocol>&lt;p>1.&amp;nbsp;Animal Housing and Treatment:&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;C57BL/6J mice were obtained at 8 weeks of age.&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;The mice were housed in a specific pathogen-free (SPF) facility with a 12-hour light/dark cycle, at a controlled temperature (22 ± 2°C) and humidity (55 ± 5%).&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;They were maintained on standard chow and water ad libitum for a period of 6 months as part of the experimental design. At the time of sacrifice, the mice were approximately 8 months old.&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;Prior to sample collection, the mice were fasted overnight for 12 hours with free access to water to minimize diet-related metabolic variations.&lt;/p>&lt;p>&lt;br>&lt;/p>&lt;p>2.&amp;nbsp;Euthanasia and Dissection:&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;Mice were euthanized by cervical dislocation, a method chosen to avoid chemical contamination of the samples.&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;The carcass was immediately placed on a clean surgical surface, and the abdominal area was sanitized with 70% ethanol.&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;Using sterile surgical instruments, the abdominal cavity was opened to expose the gastrointestinal tract.&lt;/p>&lt;p>&lt;br>&lt;/p>&lt;p>3.&amp;nbsp;Cecum Content Collection:&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;The cecum was carefully isolated from the surrounding tissues.&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;The contents of the cecum were gently squeezed into a pre-chilled and pre-labeled 2 mL sterile cryovial. Care was taken to prevent contamination from the cecal wall.&lt;/p>&lt;p>&lt;br>&lt;/p>&lt;p>4.&amp;nbsp;Sample Quenching and Storage:&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;Immediately after collection, the cryovial containing the sample was snap-frozen in liquid nitrogen to instantly halt all metabolic processes.&lt;/p>&lt;p>&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;The frozen samples were then transferred to and stored in a -80°C freezer until the metabolite extraction process.&lt;/p></sample_collection_protocol><omics_type>Metabolomics</omics_type><study_design>Periodontitis</study_design><study_design>Hyperlipidemia</study_design><study_design>guanidinopropionic acid</study_design><curator_keywords>Periodontitis</curator_keywords><curator_keywords>Hyperlipidemia</curator_keywords><curator_keywords>guanidinopropionic acid</curator_keywords><mass_spectrometry_protocol>&lt;p>Data was acquired using a Thermo Orbitrap Exploris 120 mass spectrometer with a HESI source, operating in both positive and negative ion modes. The scan range was set to 100-1000 m/z with a primary resolution of 60,000. Data-dependent acquisition (DDA) was used to collect MS/MS spectra for the top 4 ions, with a secondary resolution of 15,000 and HCD collision energy of 30%.&lt;/p></mass_spectrometry_protocol></additional><is_claimable>false</is_claimable><name>Gut commensal Odoribacter splanchnicus alleviates hyperlipidemic periodontitis via the β-GPA-TLR4 axis</name><description>&lt;p>Background: Hyperlipidemia is a well-established systemic metabolic disorder and a significant risk factor for periodontitis, a localized inflammatory condition; however, the precise mechanisms underpinning this comorbidity remain uncharacterized. Emerging evidence implicates the gut microbiota as a crucial mediator in the pathogenesis linking hyperlipidemia with periodontitis. Therefore, this study was designed to elucidate the causal role of the gut microbiota and its associated metabolic pathways in this interaction, with the ultimate goal of identifying microbiome-targeted therapeutic strategies.&lt;/p>&lt;p>Results: We found that hyperlipidemia exacerbates periodontal destruction by inducing specific gut microbiota dysbiosis. Notably, Odoribacter splanchnicus was significantly depleted in patients and mice with hyperlipidemic periodontitis (HPD). Through fecal microbiota transplantation, we established a causal link between HPD-associated gut microbiota and disease phenotypes. Oral administration of live O. splanchnicus attenuated periodontal bone loss and systemic metabolic dysfunction by remodeling the gut microbiome and upregulating the metabolite, β-guanidinopropionic acid (β-GPA). Crucially, direct supplementation with β-GPA similarly alleviated HPD phenotypes. Further mechanistic investigations revealed that β-GPA remotely inhibited the pro-inflammatory Toll-like receptor 4 (TLR4) signaling pathway in periodontal tissues.&lt;/p>&lt;p>Conclusions: Our findings establish the 'O. splanchnicus - β-GPA - TLR4' axis as a crucial protective pathway in HPD. This provides a mechanistic framework for the crosstalk between systemic metabolic disorders and local inflammatory diseases, representing an advance in microbiome-targeted therapeutic strategies for this complex comorbidity.&lt;/p>&lt;p>&lt;br>&lt;/p></description><dates><publication>2026-06-08</publication><submission>2025-10-12</submission></dates><accession>MTBLS13125</accession><cross_references/></HashMap>