Metabolites identification was performed by comparing retention time, m/z, and MS/MS spectra with an in-house reference standard library. Quantification was based on peak area relative to internal standards. Data normalization and statistical analysis were performed using R software.
"],"repository":["MetaboLights"],"study_status":["Public"],"ptm_modification":[""],"instrument_platform":["Liquid Chromatography MS - alternating - reverse-phase"],"chromatography_protocol":["The chemical composition of samples was profiled using a SCIEX system equipped with a Waters ACQUITY UPLC HSS T3 column (2.1×100 mm, 1.8 μm). The mobile phase consisted of (A) 0.1% formic acid in water and (B) acetonitrile. The gradient elution program was as follows: 0–0.5 min, 2% B; 0.5–10 min, 2–50% B; 10–11 min, 50–95% B; 11–13 min, 95% B; 13–13.1 min, 95–2% B; 13.1–15 min, 2% B. The column temperature was set at 40°C. The flow rate was 0.4 mL/min, and the injection volume was 2 µL with the autosampler maintained at 4°C.
"],"publication":["Gut microbial release of ferulic acid from germinated quinoa alleviates obesity-associated cognitive impairment via activation of PINK1/Parkin-mediated mitophagy in the hippocampus."],"submitter_name":["Yongli Lan"],"submitter_affiliation":["Northwest A&F University"],"organism_part":["seed"],"technology_type":["mass spectrometry assay"],"disease":[""],"extraction_protocol":["Sample (50 mg) was weighed into a 1.5 mL centrifuge tube. A 700 µL aliquot of a pre-cooled (-40°C) methanol/water mixture (3:1, v/v) containing the internal standard 2-chlorophenylalanine was added. The mixture was vortexed vigorously for 30 s and then homogenized using a homogenizer at 40 Hz for 4 min, followed by sonication in an ice-water bath for 5 min. This homogenization-sonication cycle was repeated three times. The sample was subsequently incubated overnight at 4°C on a thermomixer. After centrifugation at 12,000 rpm for 15 min at 4°C, the supernatant was collected, filtered through a 0.22 µm membrane, diluted five-fold with methanol/water (3:1, v/v), vortexed for 30 s, and transferred to a vial for analysis.
"],"organism":["Chenopodium quinoa"],"data_transformation_protocol":["MRM data acquisition and processing was employed on a SCIEX Analyst Work Station Software (Version 1.6.3). MS raw data (.wiff) files were converted to the TXT format using MSconventer. In-house R program and database were applied to peak detection and annotation.
"],"study_factor":["Germination"],"submitter_email":["yonglilan@nwsuaf.edu.cn"],"metabolights_link":["https://www.ebi.ac.uk/metabolights/MTBLS14185"],"sample_collection_protocol":["Quinoa seeds were firstly surface-sterilized with 4% sodium hypochlorite (5 min) and rinsed thoroughly with deionized water. After a 6-h hydration period, the seeds were placed on moist filter paper in perforated trays and germinated in the dark within a controlled climate chamber maintained at 25°C and 95% relative humidity. After 48 h of germination, the samples were then freeze-dried, ground to pass through a 100-mesh sieve, and stored at -20°C as germinated quinoa flour (germinated_quinoa ) until further analysis. Non-germinated quinoa flour (quinoa) was prepared from seeds collected at 0 h of germination. Each group included three biological replicates.
"],"omics_type":["Metabolomics"],"study_design":["ultra-performance liquid chromatography-mass spectrometry","Multi-omics study","Metabolomics","metabolite","SCIEX ExionLC AD","seed","targeted analysis","targeted metabolite profiling","microbiome","SCIEX QTRAP System","Chenopodium quinoa"],"curator_keywords":["ultra-performance liquid chromatography-mass spectrometry","Multi-omics study","Metabolomics","metabolite","SCIEX ExionLC AD","targeted analysis","seed","targeted metabolite profiling","microbiome","SCIEX QTRAP System","Chenopodium quinoa"],"mass_spectrometry_protocol":["SCIEX QTRAP 6500+ triple quadrupole mass spectrometer equipped with an IonDrive Turbo V electrospray ionization (ESI) source was performed. Mass spectrometric detection was performed in multiple reaction monitoring (MRM) mode. The ESI source parameters were set as follows: ion spray voltage, +5500/-4500 V; curtain gas, 35 psi; source temperature, 400°C; nebulizer gas (Gas 1) and auxiliary gas (Gas 2), 60 psi each; declustering potential, ±100 V.
"],"additional_accession":[]},"is_claimable":false,"name":"Gut microbial release of ferulic acid from germinated quinoa alleviates obesity-associated cognitive impairment via activation of PINK1/Parkin-mediated mitophagy in the hippocampus","description":"Background Obesity is a major risk factor for cognitive impairment and related neurodegenerative disorders. Whole grains are rich in polyphenols and dietary fiber, and their consumption has been associated with improvements in obesity and cognitive deficits. Gut microbial genes encode enzymes that metabolize dietary components, influencing host health. However, the specific microbes and enzymes involved are largely unknown. Here, we explore the potential modulating effects of dietary supplementation of germinated quinoa (GQF) on obesity-related cognitive deficits and elucidate the underlying molecular mechanisms.
Results We first found that GQF, a polyphenol-rich grain-based diet, more effectively attenuates high-fat diet-induced cognitive decline and loss of gut microbial diversity compared with native quinoa. These benefits are associated with an increased abundance of Roseburia and enrichment of carbohydrate-active enzyme gene clusters following GQF intervention. Although the neuroprotective effects of GQF are not entirely dependent on the gut microbiota, GQF selectively promotes the proliferation of feruloyl esterase (FAE)-expressing Roseburia hominis and R. intestinalis, thereby facilitating the release of free ferulic acid (FA). These findings underscore the pivotal role of gut microorganisms in mediating dietary nutritional interventions. Mechanistically, FA enhances mitophagy by activating the hippocampal PINK1/Parkin signaling pathway and increasing LC3 protein colocalization with cytochrome c (CYCS), thereby restoring synaptic structural and functional integrity.
Conclusions Collectively, our findings suggest that R. hominis and R. intestinalis, enriched by GQF intake, release bound FA via feruloyl esterase to prevent obesity-induced cognitive decline. GQF and its microbiota-derived FA can be considered a natural food-based “nutrition-microbiota-brain axis” delivery system, offering a promising therapeutic strategy for metabolic-associated cognitive impairment.
","dates":{"publication":"2026-03-30","submission":"2026-03-30"},"accession":"MTBLS14185","cross_references":{}}