MetaboLightsapplication/xmlftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13655/m_MTBLS13655_LC-MS_alternating_reverse-phase_metabolite_profiling_v2_maf.tsvftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13655/s_MTBLS13655.txtftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13655/a_MTBLS13655_LC-MS_alternating_reverse-phase_metabolite_profiling.txtftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13655/i_Investigation.txtprimaryOK200ftp://ftp.ebi.ac.uk/pub/databases/metabolights/studies/public/MTBLS13655livermass spectrometry assay<p>The parallel reaction monitoring (PRM) parameters 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.</p><p>A 25 mg aliquot of each individual sample was precisely weighed and transferred to an Eppendorf tube (Table S0). After the addition of 1000 μL of extract solution (precooled at -40 ℃, acetonitrile-methanol-water = 2:2:1, containing internal standard), the samples were vortexed for 30 s, homogenized at 35 Hz for 4 min, and sonicated for 5 min in ice-water bath. The homogenate and sonicate circle was repeated for three times, followed by incubation at -40 ℃ for 1 h and centrifugation at 12000 rpm and 4 ℃ for 15 min. The resulting supernatants were transferred to LC-MS vials for UHPLC-MS/MS analysis.</p>Rattus norvegicus<p>The parallel reaction monitoring (PRM) parameters 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.</p>Treatmenthttps://www.ebi.ac.uk/metabolights/MTBLS136553277728362@qq.com<p>The collected liver tissues were snap-frozen in liquid nitrogen, stored at -80°C, and subsequently maintained on dry ice prior to shipment for analysis.</p>MetaboLightsPublicMetabolomicsLiquid Chromatography MS - alternating - reverse-phaseBile Saltbile acid metabolic processphytosterolsDyslipidemiaGut microbiota (beta diversity)targeted metabolitesblood lipids<p>The UHPLC separation was carried out using an UHPLC System (Vanquish, Thermo Fisher Scientific), equipped with a Waters ACQUITY UPLC BEH C18 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 ℃. The auto-sampler temperature was set at 4 ℃ and the injection volume was 1 μL.</p>Dietary germ oil-derived phytosterols ameliorate hyperlipidemia by suppressing bile salt hydrolase-producing gut microbiota to enrich taurohyodeoxycholic acid.Bile Saltbile acid metabolic processphytosterolsDyslipidemiaGut microbiota (beta diversity)targeted metabolitesblood lipidsSoutheast universityJiayue Xia<p>A Orbitrap Exploris 120 mass spectrometer (Thermo Fisher Scientific) was applied for assay development. Typical ion source parameters were: 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 ℃, capillary temperature = 320 ℃.</p>falseDietary germ oil-derived phytosterols ameliorate hyperlipidemia by suppressing bile salt hydrolase-producing gut microbiota to enrich taurohyodeoxycholic acid_Bile acid profile in rat liver tissue<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.</p>2026-03-172026-01-11MTBLS13655