Patrik Rorsman

Summary

Affiliation: University of Oxford
Country: UK

Publications

  1. pmc Insulin secretion: a high-affinity Ca2+ sensor after all?
    Sebastian Barg
    The Vollum Institute, Oregon Health and Sciences University, Portland, OR 97239, USA
    J Gen Physiol 124:623-5. 2004
  2. ncbi request reprint Regulation of insulin secretion in human pancreatic islets
    Patrik Rorsman
    Oxford Center for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford OX3 7LJ, United Kingdom
    Annu Rev Physiol 75:155-79. 2013
  3. pmc Multivesicular exocytosis in rat pancreatic beta cells
    M B Hoppa
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK
    Diabetologia 55:1001-12. 2012
  4. ncbi request reprint Electrophysiology of pancreatic β-cells in intact mouse islets of Langerhans
    Patrik Rorsman
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford OX37LJ, UK
    Prog Biophys Mol Biol 107:224-35. 2011
  5. pmc Membrane potential-dependent inactivation of voltage-gated ion channels in alpha-cells inhibits glucagon secretion from human islets
    Reshma Ramracheya
    Oxford Centre for Diabetes Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
    Diabetes 59:2198-208. 2010
  6. pmc Gamma-aminobutyric acid (GABA) is an autocrine excitatory transmitter in human pancreatic beta-cells
    Matthias Braun
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
    Diabetes 59:1694-701. 2010
  7. pmc Progression of diet-induced diabetes in C57BL6J mice involves functional dissociation of Ca2(+) channels from secretory vesicles
    Stephan C Collins
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
    Diabetes 59:1192-201. 2010
  8. pmc Chronic palmitate exposure inhibits insulin secretion by dissociation of Ca(2+) channels from secretory granules
    Michael B Hoppa
    The Oxford Centre for Diabetes, Endocrinology, and Metabolism, Churchill Hospital, Oxford OX3 7LJ, UK
    Cell Metab 10:455-65. 2009
  9. pmc SSTR2 is the functionally dominant somatostatin receptor in human pancreatic β- and α-cells
    Balrik Kailey
    Oxford Centre for Diabetes, Endocrinology, and Metabolism, University of Oxford, Oxford, United Kingdom
    Am J Physiol Endocrinol Metab 303:E1107-16. 2012
  10. doi request reprint Cell coupling in mouse pancreatic beta-cells measured in intact islets of Langerhans
    Quan Zhang
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK
    Philos Trans A Math Phys Eng Sci 366:3503-23. 2008

Collaborators

Detail Information

Publications33

  1. pmc Insulin secretion: a high-affinity Ca2+ sensor after all?
    Sebastian Barg
    The Vollum Institute, Oregon Health and Sciences University, Portland, OR 97239, USA
    J Gen Physiol 124:623-5. 2004
  2. ncbi request reprint Regulation of insulin secretion in human pancreatic islets
    Patrik Rorsman
    Oxford Center for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford OX3 7LJ, United Kingdom
    Annu Rev Physiol 75:155-79. 2013
    ..Finally, we consider the pathophysiology of insulin secretion and the interactions between genetics and environmental factors that may explain the current diabetes epidemic...
  3. pmc Multivesicular exocytosis in rat pancreatic beta cells
    M B Hoppa
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK
    Diabetologia 55:1001-12. 2012
    ..To establish the occurrence, modulation and functional significance of compound exocytosis in insulin-secreting beta cells...
  4. ncbi request reprint Electrophysiology of pancreatic β-cells in intact mouse islets of Langerhans
    Patrik Rorsman
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford OX37LJ, UK
    Prog Biophys Mol Biol 107:224-35. 2011
    ..Finally, we propose a model for glucose-induced β-cell electrical activity based on observations made in intact pancreatic islets...
  5. pmc Membrane potential-dependent inactivation of voltage-gated ion channels in alpha-cells inhibits glucagon secretion from human islets
    Reshma Ramracheya
    Oxford Centre for Diabetes Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
    Diabetes 59:2198-208. 2010
    ..To document the properties of the voltage-gated ion channels in human pancreatic alpha-cells and their role in glucagon release...
  6. pmc Gamma-aminobutyric acid (GABA) is an autocrine excitatory transmitter in human pancreatic beta-cells
    Matthias Braun
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
    Diabetes 59:1694-701. 2010
    ..Paracrine signaling via gamma-aminobutyric acid (GABA) and GABA(A) receptors (GABA(A)Rs) has been documented in rodent islets. Here we have studied the importance of GABAergic signaling in human pancreatic islets...
  7. pmc Progression of diet-induced diabetes in C57BL6J mice involves functional dissociation of Ca2(+) channels from secretory vesicles
    Stephan C Collins
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
    Diabetes 59:1192-201. 2010
    ..The aim of the study was to elucidate the cellular mechanism underlying the suppression of glucose-induced insulin secretion in mice fed a high-fat diet (HFD) for 15 weeks...
  8. pmc Chronic palmitate exposure inhibits insulin secretion by dissociation of Ca(2+) channels from secretory granules
    Michael B Hoppa
    The Oxford Centre for Diabetes, Endocrinology, and Metabolism, Churchill Hospital, Oxford OX3 7LJ, UK
    Cell Metab 10:455-65. 2009
    ..In both mouse and human islets, the palmitate-induced secretion defect was reversed when the beta cell action potential was pharmacologically prolonged...
  9. pmc SSTR2 is the functionally dominant somatostatin receptor in human pancreatic β- and α-cells
    Balrik Kailey
    Oxford Centre for Diabetes, Endocrinology, and Metabolism, University of Oxford, Oxford, United Kingdom
    Am J Physiol Endocrinol Metab 303:E1107-16. 2012
    ..These effects are mediated predominantly by SSTR2 in both cell types...
  10. doi request reprint Cell coupling in mouse pancreatic beta-cells measured in intact islets of Langerhans
    Quan Zhang
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK
    Philos Trans A Math Phys Eng Sci 366:3503-23. 2008
    ....
  11. pmc A K ATP channel-dependent pathway within alpha cells regulates glucagon release from both rodent and human islets of Langerhans
    Patrick E MacDonald
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom
    PLoS Biol 5:e143. 2007
    ..We propose that elevated glucose reduces electrical activity and exocytosis via depolarisation-induced inactivation of ion channels involved in action potential firing and secretion...
  12. ncbi request reprint Muscle dysfunction caused by a KATP channel mutation in neonatal diabetes is neuronal in origin
    Rebecca H Clark
    Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK
    Science 329:458-61. 2010
    ..These findings suggest that drugs targeted against neuronal, rather than muscle, KATP channels are needed to treat the motor deficits and that such drugs require high blood-brain barrier permeability...
  13. ncbi request reprint Quantal ATP release in rat beta-cells by exocytosis of insulin-containing LDCVs
    Jovita Karanauskaite
    OCDEM, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK
    Pflugers Arch 458:389-401. 2009
    ..Our results indicate that measurements of ATP release and DeltaC(m) principally (> or =85-95%) report exocytosis of insulin granules...
  14. doi request reprint Voltage-gated ion channels in human pancreatic beta-cells: electrophysiological characterization and role in insulin secretion
    Matthias Braun
    Oxford Centre for Diabetes Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
    Diabetes 57:1618-28. 2008
    ..To characterize the voltage-gated ion channels in human beta-cells from nondiabetic donors and their role in glucose-stimulated insulin release...
  15. doi request reprint K(ATP)-channels and glucose-regulated glucagon secretion
    Patrik Rorsman
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK
    Trends Endocrinol Metab 19:277-84. 2008
    ..Here we consider the possible mechanisms involved with a focus on ATP-regulated K(+)-channels and changes in alpha-cell membrane potential...
  16. doi request reprint Exocytotic properties of human pancreatic beta-cells
    Matthias Braun
    Oxford Centre for Diabetes Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom
    Ann N Y Acad Sci 1152:187-93. 2009
    ..These results reveal both similarities and differences between human and rodent beta-cells...
  17. pmc Regulation of calcium in pancreatic α- and β-cells in health and disease
    Patrik Rorsman
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, UK
    Cell Calcium 51:300-8. 2012
    ..We also consider how subtle changes in Ca(2+)-signalling may have profound impact on β-cell performance and increase risk of developing type-2 diabetes...
  18. pmc Corelease and differential exit via the fusion pore of GABA, serotonin, and ATP from LDCV in rat pancreatic beta cells
    Matthias Braun
    Oxford Center for Diabetes, Endocrinology, and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK
    J Gen Physiol 129:221-31. 2007
    ....
  19. ncbi request reprint R-type Ca(2+)-channel-evoked CICR regulates glucose-induced somatostatin secretion
    Quan Zhang
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK
    Nat Cell Biol 9:453-60. 2007
    ..Glucose-induced somatostatin secretion is instead primarily dependent on Ca(2+)-induced Ca(2+)-release (CICR). This constitutes a novel mechanism for K(ATP)-channel-independent metabolic control of pancreatic hormone secretion...
  20. pmc Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic beta cells recapitulates neonatal diabetes
    Christophe A Girard
    Henry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK
    J Clin Invest 119:80-90. 2009
    ..2, SUR1, and insulin mRNA. All these changes are expected to contribute to the diabetes of beta-V59M mice. Their cause requires further investigation...
  21. pmc Role of KATP channels in glucose-regulated glucagon secretion and impaired counterregulation in type 2 diabetes
    Quan Zhang
    Oxford Centre for Diabetes, Endocrinology, and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK
    Cell Metab 18:871-82. 2013
    ..These data suggest that impaired metabolic control of the KATP channels underlies the defective glucose regulation of glucagon secretion in type 2 diabetes...
  22. ncbi request reprint Release of small transmitters through kiss-and-run fusion pores in rat pancreatic beta cells
    Patrick E MacDonald
    Oxford Centre for Diabetes Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, United Kingdom
    Cell Metab 4:283-90. 2006
    ..Therefore, the LDCV kiss-and-run fusion pores allow small transmitter release but likely retain the larger insulin peptide. This may represent a mechanism for selective intraislet signaling...
  23. pmc CLC-5 and KIF3B interact to facilitate CLC-5 plasma membrane expression, endocytosis, and microtubular transport: relevance to pathophysiology of Dent's disease
    Anita A C Reed
    Academic Endocrine Unit, Nuffield Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology, and Metabolism, Churchill Hospital, Oxford, United Kingdom
    Am J Physiol Renal Physiol 298:F365-80. 2010
    ..Thus, the CLC-5 and KIF3B interaction is important for CLC-5 plasma membrane expression and for facilitating endocytosis and microtubular transport in the kidney...
  24. pmc Oscillations, intercellular coupling, and insulin secretion in pancreatic beta cells
    Patrick E MacDonald
    Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom
    PLoS Biol 4:e49. 2006
  25. pmc Pathophysiological, genetic and gene expression features of a novel rodent model of the cardio-metabolic syndrome
    Robert H Wallis
    The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom
    PLoS ONE 3:e2962. 2008
    ..Complex etiology and pathogenesis of pathophysiological components of the cardio-metabolic syndrome have been demonstrated in humans and animal models...
  26. pmc Quantification of mRNA in single cells and modelling of RT-qPCR induced noise
    Martin Bengtsson
    Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, The Churchill Hospital, Oxford, OX3 7LJ, UK
    BMC Mol Biol 9:63. 2008
    ..Quantitative reverse transcription PCR (RT-qPCR) is the most accessible method which provides sufficiently accurate measurements of mRNA in single cells...
  27. pmc SEDLIN forms homodimers: characterisation of SEDLIN mutations and their interactions with transcription factors MBP1, PITX1 and SF1
    Jeshmi Jeyabalan
    Academic Endocrine Unit, Nuffield Department of Clinical Medicine, Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom
    PLoS ONE 5:e10646. 2010
    ..SEDLIN mutations cause X-linked spondyloepiphyseal dysplasia tarda (SEDT)...
  28. ncbi request reprint Diabetes mellitus and the β cell: the last ten years
    Frances M Ashcroft
    Department of Physiology, Anatomy, and Genetics, Henry Wellcome Centre for Gene Function, University of Oxford, Sherrington Building, Parks Road, Oxford OX1 3PT, UK
    Cell 148:1160-71. 2012
    ..There also have been significant advances in therapy, particularly for some monogenic disorders. We review here what ails the β cell and how its function may be restored...
  29. pmc Exocytosis from pancreatic β-cells: mathematical modelling of the exit of low-molecular-weight granule content
    Juris Galvanovskis
    Department of Physiology, Anatomy and Genetics, University of Oxford, Henry Wellcome Building, Parks Road, Oxford OX1 3PT, UK
    Interface Focus 1:143-52. 2011
    ..Our findings suggest that the fusion pore functions as a molecular sieve, allowing differential release of low- and high-molecular-weight granule constituents...
  30. doi request reprint TCF7L2 and Diabetes: A Tale of Two Tissues, and of Two Species
    Mark I McCarthy
    Oxford Centre for Diabetes, Endocrinology, and Metabolism, University of Oxford, Churchill Hospital, Old Road, Headington, Oxford OX3 7LE, UK Oxford NIHR Biomedical Research Centre, Churchill Hospital, Old Road, Headington, Oxford OX3 7LE, UK Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK Electronic address
    Cell Metab 17:157-9. 2013
    ..A recent paper in Cell (Boj et al., 2012) using rodent models to examine how diabetes-associated variants near TCF7L2 perturb metabolic regulation provides surprising results...
  31. pmc A dominant mutation in Snap25 causes impaired vesicle trafficking, sensorimotor gating, and ataxia in the blind-drunk mouse
    Alexander F Jeans
    Medical Research Council Functional Genetics Unit, University of Oxford, South Parks Road, Oxford, OX1 3QX, United Kingdom
    Proc Natl Acad Sci U S A 104:2431-6. 2007
    ..These studies therefore provide insights into the role of the SNARE complex in both diabetes and psychiatric disease...
  32. pmc Uromodulin mutations causing familial juvenile hyperuricaemic nephropathy lead to protein maturation defects and retention in the endoplasmic reticulum
    Sian E Williams
    Academic Endocrine Unit, Churchill Hospital, Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Headington, Oxford OX3 7LJ, UK
    Hum Mol Genet 18:2963-74. 2009
    ..Thus, FJHN-causing Uromodulin mutants are retained in the ER, with impaired intracellular maturation and trafficking, thereby indicating mechanisms whereby Uromodulin mutants may cause the phenotype of FJHN...