Access to the conferences will be possible by invitation in order to obtain a connection right.
Please ask for your invitation to :
Lucretia Antonia Mota (EGIR Secretary) :
Mark Walker 1 on behalf of Xuefei Yu 1, Catherine Arden 1, Chun Chen 2, Carla Bradshaw 2, Julia Whitehall 2, Michael White 1, Scott Anderson 1, James Shaw 1, Doug Turnbull 2, & Laura Greaves 2
1 Diabetes Research Group, Institute of Cellular Medicine, Faculty of Medical Science, Newcastle University, Newcastle upon Tyne, UK. 2 Wellcome Trust Mitochondrial Research Group, Institute of Neuroscience, Faculty of Medical Science, Newcastle University, Newcastle upon Tyne, UK.
Introduction: Mitochondrial DNA mutations can cause diabetes, and the accumulation of somatic mitochondrial mutations has been linked with the ageing process. The PolgA mutator mouse is a model of premature ageing. The aim of this study was to explore the relationship between mitochondrial dysfunction and islet cell composition in the PolgA mouse model.Methods: Immunofluorescence was used to study mitochondrial respiratory subunit expression (complex I and IV) and the cell composition in islets. Experiments were conducted on pancreas tissue from PolgA mice and age-matched wild type (WT) mice at 12 (young) and 44 (old) weeks of age.
Results: Complex I expression was decreased (P
Conclusions: Complex I deficiency was already present in the islets of young PolgA mice and persisted with age. This was associated with an increase in alpha cell proliferation and number in old PolgA mouse islets. We conclude that altered islet cell composition is part of the premature ageing phenotype in the PolgA mouse.
Mark Walker MD is Professor and Honorary Consultant Physician at Newcastle University and Newcastle Hospitals NHS Foundation Trust, UK. He is Director of the Newcastle NIHR Clinical Research Facility for translational research and was chair of the EASD Scientific Programme Committee from 2010-13. His research interests include the genetic basis of type 2 diabetes, mechanisms of insulin resistance, and mitochondrial diabetes.