Parkinson disease (PD) is a relatively common neurodegenerative disorder, affecting 1-2% of the world's population over the age of 65 years. About 5-10% of PD cases are inherited, and mutations in the Parkin gene are a common cause of familial PD. Michael Sack and colleagues, at the National Institutes of Health, Bethesda, have now identified a new function for the protein templated by the Parkin gene, it regulates fat uptake from the blood by liver cells and thereby fat levels in the blood. Furthermore, they determine that it does this by regulating the level of expression of the fat transporter CD36 on liver cells. Future studies will determine whether perturbations in this function of parkin contribute to the development of PD caused by mutations in the Parkin gene.
As noted in an accompanying commentary, by Nada Abumrad, at Washington University School of Medicine, St Louis, and Darren Moore, at Ecole Polytechnique Fédérale de Lausanne, Switzerland, the additional observation of Sack and colleagues that levels of parkin protein are increased in mice fed a high-fat diet, provides support for the emerging idea that dietary fat intake can impact susceptibility to PD.
TITLE: Parkin is a lipid-responsive regulator of fat uptake in mice and mutant human cells
AUTHOR CONTACT:
Michael N. Sack
National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. Phone: 301.402.9259; Fax: 301.480.4599; E-mail: sackm@nhlbi.nih.gov .
View this article at: http://www.jci.org/articles/view/44736?key=a9aa051cef209eafac0e
ACCOMPANYING COMMENTARY TITLE: Parkin reinvents itself to regulate fatty acid metabolism by tagging CD36
Nada A. Abumrad
Washington University School of Medicine, St Louis, Missouri, USA. Phone: 314.747.0348; Fax: 314.444.3432; E-mail: nabumrad@wustl.edu .
View this article at: http://www.jci.org/articles/view/59219?key=78216f975ade76ff66ad
Journal of Clinical Investigation