Volume 16, No 7, Jul 2006
ISSN: 1001-0602
EISSN: 1748-7838 2018
impact factor 17.848*
(Clarivate Analytics, 2019)
Volume 16 Issue 7, July 2006: 661-670
ORIGINAL ARTICLES
Glucose regulates LXRα subcellular localization and function in rat pancreatic β-cells
Audrey Helleboid-Chapman, Stéphane Helleboid, Heidelinde Jakel, Catherine Timmerman,Christian Sergheraert, François Pattou, Jamila Fruchart-Najib, Jean-Charles Fruchart
1Atherosclerosis Department, UR 545 INSERM, the Faculty of Pharmacy, Lille 2 University, 1 rue du Professeur Calmette BP245, Lille
cedex 59019, France; 2Synthesis, Structure and Biomolecule Function, UMR 8525 CNRS, Pasteur Institute of Lille, Lille 2 University,
Lille, France; 3Cell Therapy for Diabetes, ERIT-M 0106, Faculty of Medecine University of Lille 2/INSERM, Lille 59045, France
Correspondence: Audrey Helleboid-Chapman(audrey.chapman@pasteur-lille.fr )
Liver X receptors (LXRs) are members of the nuclear receptor superfamily, which have been implicated in lipid homeostasis
and more recently in glucose metabolism. Here, we show that glucose does not change LXRα protein level,
but affects its localization in pancreatic ?cells. LXRα is found in the nucleus at 8 mM glucose and in the cytoplasm at
4.2 mM. Addition of glucose translocates LXRα from the cytoplasm into the nucleus. Moreover, after the activation of
LXR by its synthetic non-steroidal agonist (T0901317), insulin secretion and glucose uptake are increased at 8 mM and
decreased at 4.2 mM glucose in a dose-dependent manner. Furthermore, at low glucose condition, okadaic acid reversed
LXRα effect on insulin secretion, suggesting the involvement of glucose signaling through a phosphorylation-dependent
mechanism.
Cell Research advance online publication 13 Jun 2006; doi: 10.1038/sj.cr.7310069
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