Joseph C Koster

Summary

Affiliation: Washington University School of Medicine
Country: USA

Publications

  1. pmc The G53D mutation in Kir6.2 (KCNJ11) is associated with neonatal diabetes and motor dysfunction in adulthood that is improved with sulfonylurea therapy
    Joseph C Koster
    Washington University School of Medicine, Department of Cell Biology and Physiology, Box 8228, St Louis, MO 63110, USA
    J Clin Endocrinol Metab 93:1054-61. 2008
  2. ncbi request reprint An ATP-binding mutation (G334D) in KCNJ11 is associated with a sulfonylurea-insensitive form of developmental delay, epilepsy, and neonatal diabetes
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Diabetes 56:328-36. 2007
  3. doi request reprint Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus
    Maria Sara Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Metab 9:140-51. 2009
  4. ncbi request reprint ATP-sensitive K+ channel signaling in glucokinase-deficient diabetes
    Maria S Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 54:2925-31. 2005
  5. ncbi request reprint Expression of ATP-insensitive KATP channels in pancreatic beta-cells underlies a spectrum of diabetic phenotypes
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Ave, St Louis, MO 63110, USA
    Diabetes 55:2957-64. 2006
  6. pmc Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance
    Dennis T Villareal
    Department of Medicine, Washington University School of Medicine, St Louis, Missouri, USA
    Diabetes 58:1869-78. 2009
  7. pmc Successful sulfonylurea treatment of an insulin-naïve neonate with diabetes mellitus due to a KCNJ11 mutation
    Jennifer A Wambach
    Department of Pediatrics, Washington University School of Medicine, St Louis, MO, USA
    Pediatr Diabetes 11:286-8. 2010
  8. doi request reprint K(ATP) channelopathies in the pancreas
    Maria S Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Pflugers Arch 460:307-20. 2010
  9. pmc Muscle KATP channels: recent insights to energy sensing and myoprotection
    Thomas P Flagg
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Physiol Rev 90:799-829. 2010
  10. ncbi request reprint Diabetes and insulin secretion: the ATP-sensitive K+ channel (K ATP) connection
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 54:3065-72. 2005

Collaborators

Detail Information

Publications17

  1. pmc The G53D mutation in Kir6.2 (KCNJ11) is associated with neonatal diabetes and motor dysfunction in adulthood that is improved with sulfonylurea therapy
    Joseph C Koster
    Washington University School of Medicine, Department of Cell Biology and Physiology, Box 8228, St Louis, MO 63110, USA
    J Clin Endocrinol Metab 93:1054-61. 2008
    ..2 mutations. There are two reports of improved neurological features in SU-treated DEND patients but no report of such improvement in adulthood...
  2. ncbi request reprint An ATP-binding mutation (G334D) in KCNJ11 is associated with a sulfonylurea-insensitive form of developmental delay, epilepsy, and neonatal diabetes
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Diabetes 56:328-36. 2007
    ....
  3. doi request reprint Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus
    Maria Sara Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Metab 9:140-51. 2009
    ....
  4. ncbi request reprint ATP-sensitive K+ channel signaling in glucokinase-deficient diabetes
    Maria S Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 54:2925-31. 2005
    ..The results have implications for understanding and therapy of glucokinase-related diabetes...
  5. ncbi request reprint Expression of ATP-insensitive KATP channels in pancreatic beta-cells underlies a spectrum of diabetic phenotypes
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Ave, St Louis, MO 63110, USA
    Diabetes 55:2957-64. 2006
    ..The data demonstrate that a range of phenotypes can be expected for a reduction in ATP sensitivity of beta-cell K(ATP) channels and provide models for the corollary neonatal diabetes in humans...
  6. pmc Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance
    Dennis T Villareal
    Department of Medicine, Washington University School of Medicine, St Louis, Missouri, USA
    Diabetes 58:1869-78. 2009
    ..To avoid confounding effects of hyperglycemia, insulin secretion and action were studied in subjects with the variant who had normal glucose tolerance...
  7. pmc Successful sulfonylurea treatment of an insulin-naïve neonate with diabetes mellitus due to a KCNJ11 mutation
    Jennifer A Wambach
    Department of Pediatrics, Washington University School of Medicine, St Louis, MO, USA
    Pediatr Diabetes 11:286-8. 2010
    ..Safe and effective initiation of glyburide in an insulin-naïve neonatal patient with K(ATP)-dependent PNDM argues for early detection and sulfonylurea intervention...
  8. doi request reprint K(ATP) channelopathies in the pancreas
    Maria S Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Pflugers Arch 460:307-20. 2010
    ..This review focuses on the mechanistic basis by which KATP mutations underlie insulin secretory disorders and the implications of these findings for successful clinical intervention...
  9. pmc Muscle KATP channels: recent insights to energy sensing and myoprotection
    Thomas P Flagg
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Physiol Rev 90:799-829. 2010
    ..As yet, few human diseases have been correlated with altered muscle K(ATP) activity, but genetically modified animals give important insights to likely pathological roles of aberrant channel activity in different muscle types...
  10. ncbi request reprint Diabetes and insulin secretion: the ATP-sensitive K+ channel (K ATP) connection
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 54:3065-72. 2005
    ....
  11. ncbi request reprint ATP and sulfonylurea sensitivity of mutant ATP-sensitive K+ channels in neonatal diabetes: implications for pharmacogenomic therapy
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 54:2645-54. 2005
    ..These results have important implications for the use of insulinotropic SU drugs as an alternative therapy to insulin injections...
  12. pmc DEND mutation in Kir6.2 (KCNJ11) reveals a flexible N-terminal region critical for ATP-sensing of the KATP channel
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Biophys J 95:4689-97. 2008
    ..The results reveal an important feature of the noncanonical ATP-sensing mechanism of K(ATP) channels...
  13. pmc Effects of the HIV protease inhibitor ritonavir on GLUT4 knock-out mice
    Arpita Kalla Vyas
    Department of Pediatrics, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 285:36395-400. 2010
    ..The ability of GLUT4 blockade to contribute to derangements in the other molecular pathways that influence insulin sensitivity remains to be determined...
  14. pmc Congenital hyperinsulinism and glucose hypersensitivity in homozygous and heterozygous carriers of Kir6.2 (KCNJ11) mutation V290M mutation: K(ATP) channel inactivation mechanism and clinical management
    Karen J Loechner
    Department of Pediatrics, University of North Carolina School of Medicine, Chapel Hill, USA
    Diabetes 60:209-17. 2011
    ..In this study, we sought to identify the mechanistic basis of K(ATP)-induced HI in two probands and to characterize the clinical course...
  15. ncbi request reprint Diet-induced glucose intolerance in mice with decreased beta-cell ATP-sensitive K+ channels
    Maria S Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 53:3159-67. 2004
    ....
  16. pmc HIV protease inhibitors acutely impair glucose-stimulated insulin release
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Diabetes 52:1695-700. 2003
    ..Thus, together with peripheral insulin resistance, beta-cell dysfunction likely contributes to altered glucose homeostasis associated with highly active antiretroviral therapy...
  17. pmc Critical role of gap junction coupled KATP channel activity for regulated insulin secretion
    Jonathan V Rocheleau
    Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee, USA
    PLoS Biol 4:e26. 2006
    ..Control via coupling lessens the effects of cell-cell variation and provides resistance to defects in excitability that would otherwise lead to a profound diabetic state, such as occurs in persistent neonatal diabetes mellitus...