Stable Isotope & Metabolomics Core

About Us

Services and Objectives

  • To determine metabolomic/lipidomic profiles for the diagnosis/characterization of physiological and pathophysiological states in cells, tissues and biofluids (plasma, urine, stool, etc.).
  • To perform in vivo stable isotope substrate assays to determine rates of protein synthesis, lipogenesis, peripheral glucose disposal, hepatic glucose recycling, glucose-glycerol cycling and Cori cycling, high energy phosphate (ATP, creatine phosphate) turnover, and in vitro stable isotope flux dissections of metabolic pathways.
  • To perform assessments of glycolysis (extracellular acidification rates, glycolytic ATP production rates) and mitochondrial oxygen consumption (mitochondrial respiration and mitochondrial ATP production rates) in tissue explants, primary isolated and tissue culture cells using Seahorse Biosciences Flux Analyzers.
  • To advise and instruct ES-DRC investigators and their students, fellows and technical staff in the design and interpretation of fluxomics, metabolomics/lipidomics and computational analyses with the aim of elucidating the molecular basis underlying glucose and lipid homeostasis in humans and animal models.

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Publications

  1. Y. Qiu et al., Isotopic Ratio Outlier Analysis (IROA) of the S. cerevisiae metabolome using accurate mass GC-TOF/MS: A new method for discovery. Analytical Chemistry, (2015) Accepted manuscript
  2. X. Liu et al., The Histone Demethylase KDM5 Activates Gene Expression by Recognizing Chromatin Context through Its PHD Reader Motif. Cell Reports 13, 2219-2231 (2015).
  3. N. Bonhoure et al., Loss of the RNA polymerase III repressor MAF1 confers obesity resistance. Genes & Development 29, 934-947 (2015).
  4. W. Brima et al., The brighter (and evolutionarily older) face of the metabolic syndrome: evidence from Trypanosoma cruzi infection in CD-1 mice. Diabetes-Metabolism Research and Reviews 31, 346-359 (2015).
  5. P. O. Broin et al., Intestinal Microbiota-Derived Metabolomic Blood Plasma Markers for Prior Radiation Injury. International Journal of Radiation Oncology Biology Physics 91, 360-367 (2015).
  6. J. Jao et al., Lower Preprandial Insulin and Altered Fuel Use in HIV/Antiretroviral-Exposed Infants in Cameroon. Journal of Clinical Endocrinology & Metabolism100, 3260-3269 (2015).
  7. I. J. Kurland et al., Integrative Metabolic Signatures for Hepatic Radiation Injury. Plos One 10, (2015).
  8. J. Miao et al., Hepatic insulin receptor deficiency impairs the SREBP-2 response to feeding and statins. Journal of Lipid Research 55, 659-667 (2014).
  9. R. A. Haeusler et al., Integrated control of hepatic lipogenesis versus glucose production requires FoxO transcription factors. Nature Communications 5, (2014).
  10. K. Nowak et al., Metabolomics Profiles Suggest a Mechanism for Caloric Restriction-Induced Radiation Sensitivity. International Journal of Radiation Oncology Biology Physics 90, S176-S177 (2014).
  11. B. Vaitheesvaran et al., Role of the tumor suppressor IQGAP2 in metabolic homeostasis: possible link between diabetes and cancer. Metabolomics 10, 920-937 (2014).
  12. E. S. Kim, F. Isoda, I. Kurland, C. V. Mobbs, Glucose-Induced Metabolic Memory in Schwann Cells: Prevention by PPAR Agonists. Endocrinology 154, 3054-3066 (2013).
  13. I. J. Kurland et al., Application of combined omics platforms to accelerate biomedical discovery in diabesity. Annals Meeting Reports. (2013), vol. 1287, pp. 1-16.
  14. G. Laurent et al., SIRT4 Coordinates the Balance between Lipid Synthesis and Catabolism by Repressing Malonyl CoA Decarboxylase. Molecular Cell 50, 686-698 (2013).
  15. Y. J. Yang et al., Alteration of De Novo Glucose Production Contributes to Fasting Hypoglycaemia in Fyn Deficient Mice. Plos One 8, (2013).
  16. B. Vaitheesvaran et al., Peripheral Effects of FAAH Deficiency on Fuel and Energy Homeostasis: Role of Dysregulated Lysine Acetylation. Plos One 7, (2012).
  17. X. P. Zhao et al., Regulation of lipogenesis by cyclin-dependent kinase 8-mediated control of SREBP-1. Journal of Clinical Investigation 122, 2417-2427 (2012).
  18. J. T. Haas et al., Hepatic Insulin Signaling Is Required for Obesity-Dependent Expression of SREBP-1c mRNA but Not for Feeding-Dependent Expression. Cell Metabolism 15, 873-884 (2012).
  19. Regulation of lipogenesis by cyclin-dependent kinase 8-mediated control of SREBP-1 J Clin Invest. 122(7):2417-27 (2012).
  20. Hepatic insulin signaling is required for obesity-dependent expression of SREBP-1c mRNA but not for feeding-dependent expression Cell Metab. 15(6):873-84 (2012).

 

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