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Glucose-stimulated insulin secretion correlates with beta-cell lipolysis.

Winzell MS, Ström K, Holm C, Ahrén B

Department of Clinical Sciences, Medicine, Lund University, Biomedical Center, Lund, Sweden.

BACKGROUND AND AIMS: Lipids are needed for optimal glucose-stimulated insulin secretion (GSIS), and long-chain acyl-CoA (LC-CoA) has been suggested as one candidate molecule active as a lipidic coupling factor. LC-CoAs may be available to the beta-cell via uptake of circulating free fatty acids or from hydrolysis of intracellularly stored triglycerides. Inhibition of lipolysis in rat islets using a non-specific lipase inhibitor (orlistat) resulted in blunted GSIS. The aim of this study was to investigate the relationship between GSIS and lipolysis in clonal beta-cells and in mouse islets. METHODS AND RESULTS: INS-1 cells, cultured overnight at 3.3mM or 11.1mM glucose, or freshly isolated islets were incubated with 3.3mM or 16.7mM glucose for 1h. Medium samples were collected and analyzed for insulin and glycerol. Triglycerides were measured in both INS-1 cells and islets. There was a dose-dependent glucose-stimulated lipolysis in INS-1 cells, which strongly correlated with insulin secretion (r=0.85, P<0.0001). The same phenomenon was observed in mouse islets (r=0.9, P=0.013). Low levels of triglycerides, which were observed in INS-1 cells pre-cultured at 3.3mM glucose, were associated with reduced GSIS. CONCLUSIONS: This study suggests that lipids obtained from lipolysis of intracellular triglycerides are involved in GSIS.

Published 13 March 2006 in Nutr Metab Cardiovasc Dis, 16: S11-6.
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