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Diabetes 53:S75-S78, 2004
© 2004 by the American Diabetes Association, Inc.

Section II: Beta-Cell Therapeutic Targets Other Than ATP-Sensitive K+ Channels

Liver X Receptor Activation Stimulates Insulin Secretion via Modulation of Glucose and Lipid Metabolism in Pancreatic Beta-Cells

Alexander M. Efanov, Sabine Sewing, Krister Bokvist, and Jesper Gromada

From the Lilly Research Laboratories, Hamburg, Germany

Liver X receptors (LXRs) {alpha} and ß, transcription factors of a nuclear hormone receptor family, are expressed in pancreatic islets as well as glucagon-secreting and insulin-secreting cell lines. Culture of pancreatic islets or insulin-secreting MIN6 cells with a LXR specific agonist T0901317 caused an increase in glucose-dependent insulin secretion and islet insulin content. The stimulatory effect of T0901317 on insulin secretion was observed only after >72 h of islet culture with the compound. In MIN6 cells, T0901317 increased protein expression of lipogenic enzymes, fatty acid synthase, and acetyl-CoA carboxylase. LXR activation also produced an increase in glucokinase protein and pyruvate carboxylase (PC) activity levels. The PC inhibitor phenylacetic acid abolished the increase in insulin secretion in cells treated with T0901317. The results suggest that LXRs can control insulin secretion and biosynthesis via regulation of glucose and lipid metabolism in pancreatic ß-cells.

Address correspondence and reprint requests to Dr. Alexander M. Efanov, Lilly Research Laboratories, Essener Strasse 93, D-22419 Hamburg, Germany. E-mail: efanov_alexander{at}lilly.com


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