About

Oliver Fiehn is a professor and the director of the Fiehn Lab at UC Davis. His research focuses on analytical chemistry, multi-omics, cheminformatics, and metabolomics, with applications in microbial metabolism, clinical metabolomics, agricultural and environmental chemistry, and forensics. The lab develops novel technologies, databases, and software for compound identification and data analysis in metabolomics and related fields. He has a background in analytical chemistry and leads a team that includes project scientists, postdoctoral scholars, students, and technical staff. The lab's work encompasses untargeted and targeted LC-MS/MS, GC-TOF MS, and other mass spectrometry techniques, aiming to revisit and improve metabolite identification and data interpretation. Oliver Fiehn's contributions include advancing metabolomics methodologies, developing computational tools, and fostering collaborations with international scientists and visiting scholars.

Research topics

• Biology
• Biochemistry
• Medicine
• Internal medicine
• Bioinformatics
• Chemistry
• Endocrinology
• Psychology
• Pharmacology
• Genetics
• Psychiatry
• Neuroscience
• Microbiology
• Physical therapy
• Chromatography
• Organic chemistry
• Immunology
• Biophysics
• Physiology
• Cell biology
• Botany
• Intensive care medicine

Selected publications

• Predicting chronic postsurgical pain: current evidence and a novel program to develop predictive biomarker signatures

  Pain · 2023 · 101 citations

  • Medicine
  • Bioinformatics
  • Intensive care medicine

  ABSTRACT: Chronic pain affects more than 50 million Americans. Treatments remain inadequate, in large part, because the pathophysiological mechanisms underlying the development of chronic pain remain poorly understood. Pain biomarkers could potentially identify and measure biological pathways and phenotypical expressions that are altered by pain, provide insight into biological treatment targets, and help identify at-risk patients who might benefit from early intervention. Biomarkers are used to diagnose, track, and treat other diseases, but no validated clinical biomarkers exist yet for chronic pain. To address this problem, the National Institutes of Health Common Fund launched the Acute to Chronic Pain Signatures (A2CPS) program to evaluate candidate biomarkers, develop them into biosignatures, and discover novel biomarkers for chronification of pain after surgery. This article discusses candidate biomarkers identified by A2CPS for evaluation, including genomic, proteomic, metabolomic, lipidomic, neuroimaging, psychophysical, psychological, and behavioral measures. Acute to Chronic Pain Signatures will provide the most comprehensive investigation of biomarkers for the transition to chronic postsurgical pain undertaken to date. Data and analytic resources generatedby A2CPS will be shared with the scientific community in hopes that other investigators will extract valuable insights beyond A2CPS's initial findings. This article will review the identified biomarkers and rationale for including them, the current state of the science on biomarkers of the transition from acute to chronic pain, gaps in the literature, and how A2CPS will address these gaps.

  DOI

• An adaptive teosinte <i>mexicana</i> introgression modulates phosphatidylcholine levels and is associated with maize flowering time

  Proceedings of the National Academy of Sciences · 2022 · 46 citations

  • Biology
  • Genetics
  • Botany

  underlies a large metabolic QTL that modulates phosphatidylcholine levels and has an adaptive effect at least in part via induction of early flowering time.

  DOI

• Intestinal α1-2-Fucosylation Contributes to Obesity and Steatohepatitis in Mice

  Cellular and Molecular Gastroenterology and Hepatology · 2021 · 29 citations

  • Endocrinology
  • Internal medicine
  • Biology

  BACKGROUND & AIMS: Fucosyltransferase 2 (Fut2)-mediated intestinal α1- 2-fucosylation is important for host-microbe interactions and has been associated with several diseases, but its role in obesity and hepatic steatohepatitis is not known. The aim of this study was to investigate the role of Fut2 in a Western-style diet-induced mouse model of obesity and steatohepatitis. METHODS: Wild-type (WT) and Fut2-deficient littermate mice were used and features of the metabolic syndrome and steatohepatitis were assessed after 20 weeks of Western diet feeding. RESULTS: Intestinal α1-2-fucosylation was suppressed in WT mice after Western diet feeding, and supplementation of α1-2-fucosylated glycans exacerbated obesity and steatohepatitis in these mice. Fut2-deficient mice were protected from Western diet-induced features of obesity and steatohepatitis despite an increased caloric intake. These mice have increased energy expenditure and thermogenesis, as evidenced by a higher core body temperature. Protection from obesity and steatohepatitis associated with Fut2 deficiency is transmissible to WT mice via microbiota exchange; phenotypic differences between Western diet-fed WT and Fut2-deficient mice were reduced with antibiotic treatment. Fut2 deficiency attenuated diet-induced bile acid accumulation by altered relative abundance of bacterial enzyme 7-α-hydroxysteroid dehydrogenases metabolizing bile acids and by increased fecal excretion of secondary bile acids. This also was associated with increased intestinal farnesoid X receptor/fibroblast growth factor 15 signaling, which inhibits hepatic synthesis of bile acids. Dietary supplementation of α1-2-fucosylated glycans abrogates the protective effects of Fut2 deficiency. CONCLUSIONS: α1-2-fucosylation is an important host-derived regulator of intestinal microbiota and plays an important role for the pathogenesis of obesity and steatohepatitis in mice.

  DOI

• Alterations in acylcarnitines, amines, and lipids inform about the mechanism of action of citalopram/escitalopram in major depression

  Translational Psychiatry · 2021 · 96 citations

  • Internal medicine
  • Endocrinology
  • Pharmacology

  ). Remitters exhibited (a) higher baseline levels of C3, C5, alpha-aminoadipic acid, sarcosine, and serotonin; and (b) higher week-8 levels of PC aa C34:1, PC aa C34:2, PC aa C36:2, and PC aa C36:4. These findings suggest that mitochondrial energetics-including acylcarnitine metabolism, transport, and its link to β-oxidation-and lipid membrane remodeling may play roles in SSRI treatment response.

  PublisherOA PDFDOI

• A Cardiovascular Disease-Linked Gut Microbial Metabolite Acts via Adrenergic Receptors

  Cell · 2020 · 725 citations

  • Biology
  • Pharmacology
  • Internal medicine
  DOI

• Structure of human GABAB receptor in an inactive state

  Nature · 2020 · 98 citations

  • Cell biology
  • Chemistry
  • Biophysics
  DOI

• A non-hallucinogenic psychedelic analogue with therapeutic potential

  Nature · 2020 · 457 citations

  • Pharmacology
  • Medicine
  • Neuroscience
  DOI

• Metabolic Network Analysis Reveals Altered Bile Acid Synthesis and Metabolism in Alzheimer’s Disease

  Cell Reports Medicine · 2020 · 206 citations

  • Biology
  • Biochemistry
  • Internal medicine

  Increasing evidence suggests Alzheimer's disease (AD) pathophysiology is influenced by primary and secondary bile acids, the end product of cholesterol metabolism. We analyze 2,114 post-mortem brain transcriptomes and identify genes in the alternative bile acid synthesis pathway to be expressed in the brain. A targeted metabolomic analysis of primary and secondary bile acids measured from post-mortem brain samples of 111 individuals supports these results. Our metabolic network analysis suggests that taurine transport, bile acid synthesis, and cholesterol metabolism differ in AD and cognitively normal individuals. We also identify putative transcription factors regulating metabolic genes and influencing altered metabolism in AD. Intriguingly, some bile acids measured in brain tissue cannot be explained by the presence of enzymes responsible for their synthesis, suggesting that they may originate from the gut microbiome and are transported to the brain. These findings motivate further research into bile acid metabolism in AD to elucidate their possible connection to cognitive decline.

  DOI

• Thioproline formation as a driver of formaldehyde toxicity in <i>Escherichia coli</i>

  Biochemical Journal · 2020 · 23 citations

  • Chemistry
  • Biochemistry
  • Biology

  Formaldehyde (HCHO) is a reactive carbonyl compound that formylates and cross-links proteins, DNA, and small molecules. It is of specific concern as a toxic intermediate in the design of engineered pathways involving methanol oxidation or formate reduction. The interest in engineering these pathways is not, however, matched by engineering-relevant information on precisely why HCHO is toxic or on what damage-control mechanisms cells deploy to manage HCHO toxicity. The only well-defined mechanism for managing HCHO toxicity is formaldehyde dehydrogenase-mediated oxidation to formate, which is counterproductive if HCHO is a desired pathway intermediate. We therefore sought alternative HCHO damage-control mechanisms via comparative genomic analysis. This analysis associated homologs of the Escherichia coli pepP gene with HCHO-related one-carbon metabolism. Furthermore, deleting pepP increased the sensitivity of E. coli to supplied HCHO but not other carbonyl compounds. PepP is a proline aminopeptidase that cleaves peptides of the general formula X-Pro-Y, yielding X + Pro-Y. HCHO is known to react spontaneously with cysteine to form the close proline analog thioproline (thiazolidine-4-carboxylate), which is incorporated into proteins and hence into proteolytic peptides. We therefore hypothesized that certain thioproline-containing peptides are toxic and that PepP cleaves these aberrant peptides. Supporting this hypothesis, PepP cleaved the model peptide Ala-thioproline-Ala as efficiently as Ala-Pro-Ala in vitro and in vivo, and deleting pepP increased sensitivity to supplied thioproline. Our data thus (i) provide biochemical genetic evidence that thioproline formation contributes substantially to HCHO toxicity and (ii) make PepP a candidate damage-control enzyme for engineered pathways having HCHO as an intermediate.

  DOI

• A lipidome atlas in MS-DIAL 4

  Nature Biotechnology · 2020 · 853 citations

  • Chemistry
  • Chromatography
  • Biochemistry
  DOI

Recent grants

• METABOLOMICS: Integrating cheminformatic resources for investigating photoautotrophic and mixotrophic metabolism in algae.

  NSF · $2.5M · 2011–2018

• West Coast Central Comprehensive Metabolomics Resource Core (WC3MRC)

  NIH · $19.7M · 2012–2019

• NIH Grant R01ES013932

  NIH · $2.2M · 2011

• Collaborative Research: Metabolite damage - A stumbling block for synthetic biology

  NSF · $370k · 2016–2021

• Integrating metagenomics data into accurate mass stool metabolite identifications

  NIH · $319k · 2022–2024

Frequent coauthors

• Rima Kaddurah‐Daouk

  Duke University

  327 shared

• Rebecca Baillie

  Rosa (United States)

  223 shared

• Stephen T. Turner

  Australian Regenerative Medicine Institute

  195 shared

• Reginald F. Frye

  University of Florida Health Science Center

  194 shared

• Eric Boerwinkle

  The University of Texas Health Science Center at Houston

  193 shared

• Yan Gong

  University of Florida

  193 shared

• Julie A. Johnson

  University of North Carolina at Chapel Hill

  192 shared

• Rhonda M. Cooper‐DeHoff

  University of Florida

  192 shared

Labs

• Fiehn LabPI

Education

• PhD, Water Quality Control

  Technical University Berlin, Germany

  1997

Similar researchers at University of California, Davis

• Blake Meyersh-126
• J. Bruce Germanh-114
• John Douglas McPhersonh-108
• Steven J. Luckh-104
• Paul J. Hagermanh-99