<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/MTBLS13654/m_MTBLS13654_LC-MS_alternating_reverse-phase_metabolite_profiling_v2_maf.tsv</Tabular><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13654/s_MTBLS13654.txt</Txt><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13654/i_Investigation.txt</Txt><Txt>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13654/a_MTBLS13654_LC-MS_alternating_reverse-phase_metabolite_profiling.txt</Txt></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><ftp_download_link>ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13654</ftp_download_link><organism_part>serum</organism_part><technology_type>mass spectrometry assay</technology_type><metabolite_identification_protocol>&lt;p>The&amp;nbsp;parallel reaction monitoring (PRM) parameters&amp;nbsp;for each of the targeted analytes were optimized, by injecting the standard solutions of the individual analytes, into the API source of the mass spectrometer. Since most of the analytes did not show product ion acceptable for quantification, the precursor ion in high resolution was selected for quantification.&lt;/p></metabolite_identification_protocol><disease></disease><extraction_protocol>&lt;p>100&amp;nbsp;μL of sample was transferred to an EP tube. After the addition of 400&amp;nbsp;μL of extract solvent (acetonitrile-methanol =1:1,&amp;nbsp;containing internal standard), the samples were vortexed for 30 s, sonicated for 10 min in ice-water bath followed by incubation at -40&amp;nbsp;oC&amp;nbsp;for 1 h and&amp;nbsp;centrifugation at 12000 rpm and 4&amp;nbsp;oC&amp;nbsp;for 15 min. The clear supernatants were transferred to an auto-sampler vial for UHPLC-MS/MS analysis.&lt;/p></extraction_protocol><organism>Homo sapiens</organism><data_transformation_protocol>&lt;p>The&amp;nbsp;parallel reaction monitoring (PRM) parameters&amp;nbsp;for each of the targeted analytes were optimized, by injecting the standard solutions of the individual analytes, into the API source of the mass spectrometer. Since most of the analytes did not show product ion acceptable for quantification, the precursor ion in high resolution was selected for quantification.&lt;/p></data_transformation_protocol><study_factor>Treatment</study_factor><metabolights_link>https://www.ebi.ac.uk/metabolights/MTBLS13654</metabolights_link><submitter_email>3277728362@qq.com</submitter_email><sample_collection_protocol>&lt;p>After centrifugation of the collected whole blood, a portion of the serum was aliquoted into cryovials, stored on dry ice, and subsequently subjected to analysis.&lt;/p></sample_collection_protocol><repository>MetaboLights</repository><study_status>Public</study_status><ptm_modification></ptm_modification><omics_type>Metabolomics</omics_type><instrument_platform>Liquid Chromatography MS - alternating - reverse-phase</instrument_platform><study_design>Bile Salt</study_design><study_design>bile acid metabolic process</study_design><study_design>phytosterols</study_design><study_design>Dyslipidemia</study_design><study_design>Gut microbiota (beta diversity)</study_design><study_design>targeted metabolites</study_design><study_design>blood lipids</study_design><chromatography_protocol>&lt;p>The UHPLC separation was carried out using an UHPLC System (Vanquish, Thermo Fisher Scientific), equipped with a Waters ACQUITY UPLC&amp;nbsp;BEH C18&amp;nbsp;column (150 all_fetch_status all_status eb_eye_copy_status eb_eye_entry_counts eb_eye_fetch_status eb_eye_metabolights_compounds.copy eb_eye_metabolights_studies.copy e_fetch_status europe_PMC_metabolights_studies.copy europe_PMC_metabolights_studies.xml studies.copy study.xml tail.xml thomsonreuters_metabolights_studies.copy thomsonreuters_metabolights_studies.xml 2.1 mm, 1.7 μm, Waters). The mobile phase A was 5 mmol/L ammonium acetate in water, and the mobile phase B was acetonitrile. The column temperature was set at 45&amp;nbsp;℃. The auto-sampler temperature was set at 4&amp;nbsp;℃&amp;nbsp;and the injection volume was 1 μL.&lt;/p></chromatography_protocol><publication>Dietary germ oil-derived phytosterols ameliorate hyperlipidemia by suppressing bile salt hydrolase-producing gut microbiota to enrich taurohyodeoxycholic acid.</publication><curator_keywords>Bile Salt</curator_keywords><curator_keywords>bile acid metabolic process</curator_keywords><curator_keywords>phytosterols</curator_keywords><curator_keywords>Dyslipidemia</curator_keywords><curator_keywords>Gut microbiota (beta diversity)</curator_keywords><curator_keywords>targeted metabolites</curator_keywords><curator_keywords>blood lipids</curator_keywords><submitter_affiliation>Southeast university</submitter_affiliation><submitter_name>Jiayue Xia</submitter_name><mass_spectrometry_protocol>&lt;p>A&amp;nbsp;Orbitrap Exploris 120&amp;nbsp;mass spectrometer (Thermo Fisher Scientific) was applied for assay development. Typical ion source parameters were:&amp;nbsp;spray voltage = +3500/-3200 V, sheath gas (N2) flow rate = 40, aux gas (N2) flow rate = 15, sweep gas (N2) flow rate = 0, aux gas (N2) temperature = 350&amp;nbsp;℃,&amp;nbsp;capillary temperature = 320&amp;nbsp;℃.&lt;/p></mass_spectrometry_protocol></additional><is_claimable>false</is_claimable><name>Dietary germ oil-derived phytosterols ameliorate hyperlipidemia by suppressing bile salt hydrolase-producing gut microbiota to enrich taurohyodeoxycholic acid_Serum bile acids in individuals with dyslipidemia</name><description>&lt;p>Dyslipidemia is a major cardiovascular risk factor. While dietary phytosterols are known to lower cholesterol, the mechanisms involving the gut-liver axis are not fully understood. By integrating human clinical trials and mechanistic animal models, we demonstrate that phytosterols improve lipid profiles by modulating the gut microbiota-bile acid-farnesoid X receptor (FXR) axis. Phytosterol supplementation suppresses the abundance of bile salt hydrolase-active bacteria, such as Lactobacillus, leading to reduced intestinal enzymatic activity and the accumulation of conjugated bile acids. These bile acids act as intestinal FXR antagonists, downregulating the ileal fibroblast growth factor 15 (FGF15) signaling pathway. This suppression relieves feedback inhibition on hepatic bile acid synthesis, thereby accelerating cholesterol catabolism. Fecal microbiota transplantation validates that these metabolic benefits are gut microbiota dependent. Together, these findings link dietary phytosterols to host lipid metabolism through gut microbial bile acid regulation, providing a mechanistic framework for individualized, food-based strategies to manage dyslipidemia.&lt;/p></description><dates><publication>2026-03-17</publication><submission>2026-01-11</submission></dates><accession>MTBLS13654</accession><cross_references/></HashMap>