UCL  IRIS
Institutional Research Information Service
UCL Logo
Please report any queries concerning the funding data grouped in the sections named "Externally Awarded" or "Internally Disbursed" (shown on the profile page) to your Research Finance Administrator. Your can find your Research Finance Administrator at https://www.ucl.ac.uk/finance/research/rs-contacts.php by entering your department
Please report any queries concerning the student data shown on the profile page to:

Email: portico-services@ucl.ac.uk

Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
Publication Detail
PINK1 deficiency in β-cells increases basal insulin secretion and improves glucose tolerance in mice.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Deas E, Piipari K, Machhada A, Li A, Gutierrez-del-Arroyo A, Withers DJ, Wood NW, Abramov AY
  • Publication date:
    07/05/2014
  • Pagination:
    140051, ?
  • Journal:
    Open Biol
  • Volume:
    4
  • Status:
    Published online
  • Country:
    England
  • PII:
    rsob.140051
  • Language:
    eng
  • Keywords:
    PINK1, Parkinson's disease, diabetes, insulin, β-cells, Animals, Calcium, Cells, Cultured, Diabetes Mellitus, Experimental, Glucose, Glucose Tolerance Test, Insulin, Insulin-Secreting Cells, Islets of Langerhans, Mice, Mice, Knockout, Mitochondria, Protein Kinases, RNA Interference, RNA, Small Interfering, Reactive Oxygen Species
Abstract
The Parkinson's disease (PD) gene, PARK6, encodes the PTEN-induced putative kinase 1 (PINK1) mitochondrial kinase, which provides protection against oxidative stress-induced apoptosis. Given the link between glucose metabolism, mitochondrial function and insulin secretion in β-cells, and the reported association of PD with type 2 diabetes, we investigated the response of PINK1-deficient β-cells to glucose stimuli to determine whether loss of PINK1 affected their function. We find that loss of PINK1 significantly impairs the ability of mouse pancreatic β-cells (MIN6 cells) and primary intact islets to take up glucose. This was accompanied by higher basal levels of intracellular calcium leading to increased basal levels of insulin secretion under low glucose conditions. Finally, we investigated the effect of PINK1 deficiency in vivo and find that PINK1 knockout mice have improved glucose tolerance. For the first time, these combined results demonstrate that loss of PINK1 function appears to disrupt glucose-sensing leading to enhanced insulin release, which is uncoupled from glucose uptake, and suggest a key role for PINK1 in β-cell function.
Publication data is maintained in RPS. Visit https://rps.ucl.ac.uk
 More search options
UCL Researchers
Author
Clinical and Movement Neurosciences
Author
Clinical and Movement Neurosciences
Author
Clinical and Movement Neurosciences
University College London - Gower Street - London - WC1E 6BT Tel:+44 (0)20 7679 2000

© UCL 1999–2011

Search by