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Cecilia Holm

Professor

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

Author

  • Maria Sörhede Winzell
  • Kristoffer Ström
  • Cecilia Holm
  • Bo Ahrén

Summary, in English

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-cell and in mouse islets. Methods and results: INS-1 cells, cultured overnight at 3.3 mM or 11.1 mM glucose, or freshly isolated islets were incubated with 3.3 mM, or 16.7 mM glucose for 1 h. 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 3.3 mM glucose, were associated with reduced GSIS. Conclusions: This study suggests that lipids obtained from lipolysis of intracellular triglycerides are involved in GSIS. (c) 2005 Elsevier B.V. All rights reserved.

Department/s

  • Medicine, Lund
  • Molecular Endocrinology

Publishing year

2006

Language

English

Pages

11-16

Publication/Series

Nutrition Metabolism and Cardiovascular Diseases

Volume

16

Document type

Journal article

Publisher

Elsevier

Topic

  • Cardiac and Cardiovascular Systems

Keywords

  • insulin secretion
  • glycerol
  • islets
  • INS-1 cells
  • triglycerides

Status

Published

Research group

  • Molecular Endocrinology

ISBN/ISSN/Other

  • ISSN: 1590-3729