Can we predict who is at risk of facing cognitive issues in PD and address them earlier? These are the questions being pursued by Dr. Goldman of the PDF Research Center at Rush University Medical Center.
PDF Grant Programs
Are you interested in furthering Parkinson's science? View PDF's open grant programs.
PINK1 deficiency in b-cells increases basal insulin secretion and improves glucose tolerance in mice.
PDF's targeted PubMed search provides you with access to journal articles from the last 90 days that may be pertinent to Parkinson's disease research.
Not what you're looking for? Do you need informational publications about Parkinson's targeted for people living with Parkinson's, caregivers and family members? Please browse PDF's educational materials and programs - which are all available electronically or in print. Order for yourself, a loved one or in bulk for your patients or support group.
Open Biol 2014 May; 4(5):140051
Authors: Emma Deas, Kaisa Piipari, Asif Machhada, Abi Li, Ana Gutierrez-del-Arroyo, Dominic J Withers, Nicholas W Wood, Andrey Y Abramov
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 ?-cells, and the reported association of PD with type 2 diabetes, we investigated the response of PINK1-deficient ?-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 ?-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 ?-cell function.
PMID: 24941499 [PubMed - as supplied by publisher]