Research Topics
Genomes and Genes | Patrik RorsmanSummaryAffiliation: University of Oxford Country: UK Publications
| Collaborators
|
Detail Information
Publications
Regulation of insulin secretion in human pancreatic isletsPatrik 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...
Multivesicular exocytosis in rat pancreatic beta cellsM 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...- Oscillations, intercellular coupling, and insulin secretion in pancreatic beta cellsPatrick E MacDonald
Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom
PLoS Biol 4:e49. 2006 - Electrophysiology of pancreatic β-cells in intact mouse islets of LangerhansPatrik 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... - Membrane potential-dependent inactivation of voltage-gated ion channels in alpha-cells inhibits glucagon secretion from human isletsReshma 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... - Gamma-aminobutyric acid (GABA) is an autocrine excitatory transmitter in human pancreatic beta-cellsMatthias 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... - Progression of diet-induced diabetes in C57BL6J mice involves functional dissociation of Ca2(+) channels from secretory vesiclesStephan 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... - Chronic palmitate exposure inhibits insulin secretion by dissociation of Ca(2+) channels from secretory granulesMichael 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... - A K ATP channel-dependent pathway within alpha cells regulates glucagon release from both rodent and human islets of LangerhansPatrick 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... - Cell coupling in mouse pancreatic beta-cells measured in intact islets of LangerhansQuan 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.... - Muscle dysfunction caused by a KATP channel mutation in neonatal diabetes is neuronal in originRebecca 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... - Quantal ATP release in rat beta-cells by exocytosis of insulin-containing LDCVsJovita 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... - Voltage-gated ion channels in human pancreatic beta-cells: electrophysiological characterization and role in insulin secretionMatthias 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... - K(ATP)-channels and glucose-regulated glucagon secretionPatrik 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... - Regulation of calcium in pancreatic α- and β-cells in health and diseasePatrik 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... - Corelease and differential exit via the fusion pore of GABA, serotonin, and ATP from LDCV in rat pancreatic beta cellsMatthias Braun
Oxford Center for Diabetes, Endocrinology, and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK
J Gen Physiol 129:221-31. 2007.... - Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic beta cells recapitulates neonatal diabetesChristophe 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... - Exocytotic properties of human pancreatic beta-cellsMatthias 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... 
R-type Ca(2+)-channel-evoked CICR regulates glucose-induced somatostatin secretionQuan 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...- CLC-5 and KIF3B interact to facilitate CLC-5 plasma membrane expression, endocytosis, and microtubular transport: relevance to pathophysiology of Dent's diseaseAnita 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... - Release of small transmitters through kiss-and-run fusion pores in rat pancreatic beta cellsPatrick 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... - Pathophysiological, genetic and gene expression features of a novel rodent model of the cardio-metabolic syndromeRobert 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... - Quantification of mRNA in single cells and modelling of RT-qPCR induced noiseMartin 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... - SEDLIN forms homodimers: characterisation of SEDLIN mutations and their interactions with transcription factors MBP1, PITX1 and SF1Jeshmi 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)... - Diabetes mellitus and the β cell: the last ten yearsFrances 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... - Exocytosis from pancreatic β-cells: mathematical modelling of the exit of low-molecular-weight granule contentJuris 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... - A dominant mutation in Snap25 causes impaired vesicle trafficking, sensorimotor gating, and ataxia in the blind-drunk mouseAlexander 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... - Uromodulin mutations causing familial juvenile hyperuricaemic nephropathy lead to protein maturation defects and retention in the endoplasmic reticulumSian 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...