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The dynamin-related GTPase Opa1 is required for glucose-stimulated ATP production in pancreatic beta cells.

Previous studies using in vitro cell culture systems have shown the role of the dynamin-related GTPase Opa1 in apoptosis prevention and mitochondrial DNA (mtDNA) maintenance. However, it remains to be tested whether these functions of Opa1 are physiologically important in vivo in mammals. Here, using the Cre-loxP system, we deleted mouse Opa1 in pancreatic beta cells, in which glucose-stimulated ATP production in mitochondria plays a key role in insulin secretion. Beta cells lacking Opa1 maintained normal copy numbers of mtDNA; however, the amount and activity of electron transport chain complex IV were significantly decreased, leading to impaired glucose-stimulated ATP production and insulin secretion. In addition, in Opa1-null beta cells, cell proliferation was impaired, whereas apoptosis was not promoted. Consequently, mice lacking Opa1 in beta cells develop hyperglycemia. The data suggest that the function of Opa1 in the maintenance of the electron transport chain is physiologically relevant in beta cells.

Pubmed ID: 21551073


  • Zhang Z
  • Wakabayashi N
  • Wakabayashi J
  • Tamura Y
  • Song WJ
  • Sereda S
  • Clerc P
  • Polster BM
  • Aja SM
  • Pletnikov MV
  • Kensler TW
  • Shirihai OS
  • Iijima M
  • Hussain MA
  • Sesaki H


Molecular biology of the cell

Publication Data

July 1, 2011

Associated Grants

  • Agency: NIDDK NIH HHS, Id: DK079639
  • Agency: NIDDK NIH HHS, Id: DK081472
  • Agency: NIGMS NIH HHS, Id: GM084015
  • Agency: NIGMS NIH HHS, Id: GM089853
  • Agency: NIDDK NIH HHS, Id: R01 DK035914
  • Agency: NIGMS NIH HHS, Id: R01 GM084015
  • Agency: NIGMS NIH HHS, Id: R01 GM089853
  • Agency: NIGMS NIH HHS, Id: R01 GM089853-01A1
  • Agency: NIGMS NIH HHS, Id: R01 GM089853-02

Mesh Terms

  • Adenosine Triphosphate
  • Animals
  • Apoptosis
  • Cell Proliferation
  • DNA, Mitochondrial
  • Dynamins
  • Electron Transport Complex IV
  • GTP Phosphohydrolases
  • Glucose
  • Glucose Intolerance
  • Hyperglycemia
  • Insulin
  • Insulin-Secreting Cells
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mitochondria
  • Receptor-Interacting Protein Serine-Threonine Kinases