Clinical Focus

  • Cardiovascular Disease

Academic Appointments

Professional Education

  • Medical Education: Stanford University School of Medicine (2009) CA
  • Residency: Stanford University Internal Medicine Residency (2012) CA
  • Board Certification: American Board of Internal Medicine, Advanced Heart Failure and Transplant Cardiology (2016)
  • Fellowship: Stanford University Cardiovascular Medicine Fellowship (2017) CA
  • Board Certification: American Board of Internal Medicine, Cardiovascular Disease (2016)
  • Fellowship: Stanford University Cardiovascular Medicine Fellowship (2016) CA
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2012)

All Publications

  • HIF-1 regulates hypoxia- and insulin-induced expression of apelin in adipocytes AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM Glassford, A. J., Yue, P., Sheikh, A. Y., Chun, H. J., Zarafshar, S., Chan, D. A., Reaven, G. M., Quertermous, T., Tsao, P. S. 2007; 293 (6): E1590-E1596


    Apelin, a novel peptide with significant cardioactive properties, is upregulated by insulin in adipocytes. However, the mechanism by which insulin promotes apelin production is unknown. Hypoxia-inducible factor-1 (HIF-1), a heterodimeric transcription factor involved in the angiogenic and metabolic responses to tissue hypoxia, has been shown to be activated by insulin in various settings. We therefore hypothesized that HIF-1 regulates insulin-mediated apelin expression in adipocytes. 3T3-L1 cells were differentiated into adipocytes in culture. For experiments, serum-starved 3T3-L1 cells were exposed to insulin and/or a 1% O(2) environment. Apelin expression was assessed using quantitative real-time PCR and ELISA. To directly assess the role of HIF-1 in apelin production, we differentiated mouse embryonic fibroblasts (MEFs) containing a targeted deletion of the HIF-1alpha gene into adipocytes and measured their response to insulin and hypoxia. Apelin expression in mature 3T3-L1 adipocytes was increased significantly by insulin and was attenuated by pharmacological inhibition of insulin signaling. Exposure of cells to either hypoxia or the chemical HIF activators cobalt chloride (CoCl(2)) and dimethyloxaloylglycine (DMOG) resulted in significant upregulation of apelin, consistent with a role for HIF in apelin induction. Moreover, hypoxia-, CoCl(2)-, DMOG-, and insulin-induced apelin expression were all attenuated in differentiated HIF-1alpha-deficient MEFs. In summary, in cultured 3T3-L1 adipocytes and differentiated MEFs, HIF-1 appears to be involved in hypoxia- and insulin-induced apelin expression.

    View details for DOI 10.1152/ajpendo.00490.2007

    View details for Web of Science ID 000251510200014

    View details for PubMedID 17878221

    View details for PubMedCentralID PMC2570255