Elevated insulin secretion from liver X receptor-activated pancreatic beta-cells involves increased de novo lipid synthesis and triacylglyceride turnover.

ABSTRACT: Increased basal and loss of glucose-stimulated insulin secretion (GSIS) are hallmarks of beta-cell dysfunction associated with type 2 diabetes. It has been proposed that elevated glucose promotes insulin secretory defects by activating sterol regulatory element binding protein (SREBP)-1c, lipogenic gene expression, and neutral lipid storage. Activation of liver X receptors (LXRs) also activates SREBP-1c and increases lipogenic gene expression and neutral lipid storage but increases basal and GSIS. This study was designed to characterize the changes in de novo fatty acid and triacylglyceride (TAG) synthesis in LXR-activated beta-cells and determine how these changes contribute to elevated basal and GSIS. Treatment of INS-1 beta-cells with LXR agonist T0901317 and elevated glucose led to mar

SUBMITTER: Green CD 

PROVIDER: S-EPMC2689804 | biostudies-literature | 2009 Jun

REPOSITORIES: biostudies-literature