Cited by 133Pancreatic function and diabetesMitochondrial Function and PathologyMetabolism, Diabetes, and Cancer

Mitochondrial signals drive insulin secretion in the pancreatic β-cell

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Wiederkehr, Andreas, Wollheim, Claes B.·2012·Molecular and Cellular Endocrinology

Abstract

β-Cell nutrient sensing depends on mitochondrial function. Oxidation of nutrient-derived metabolites in the mitochondria leads to plasma membrane depolarization, Ca(2+) influx and insulin granule exocytosis. Subsequent mitochondrial Ca(2+) uptake further accelerates metabolism and oxidative phosphorylation. Nutrient activation also increases the mitochondrial matrix pH. This alkalinization is required to maintain elevated insulin secretion during prolonged nutrient stimulation. Together the mitochondrial Ca(2+) rise and matrix alkalinization assure optimal ATP synthesis necessary for efficient activation of the triggering pathway of insulin secretion. The sustained, amplifying pathway of insulin release also depends on mitochondrial Ca(2+) signals, which likely influence the generation of glucose-derived metabolites serving as coupling factors. Therefore, mitochondria are both recipients and generators of signals essential for metabolism-secretion coupling. Activation of these signaling pathways would be an attractive target for the improvement of β-cell function and the treatment of type 2 diabetes.

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Crossref · 10.1016/j.mce.2011.07.016

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  • Mitochondria fulfill a crucial role in determining cellular, tissue, and systemic metabolic flexibility.

    “Additionally, insulin secretion from pancreatic β cells (104) and synthesis and secretion of adipokines from WAT is dependent on mitochondrial function (105), suggesting that mitochondria fulfill a crucial role in determining cellular, tissue, and systemic metabolic flexibility.”

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Authors
Wiederkehr, A., & Wollheim, C. B.
Affiliations
University of Geneva (CH)
Corresponding author
  • Wiederkehr, Andreas
  • Wollheim, Claes B.
Venue
Molecular and Cellular Endocrinology
Publisher
Elsevier BV
Published
2012-04
Volume
353
Issue
1-2
Pages
128-137
ISSN
0303-7207 (ISSN-L)
OpenAlex
W2040651543
Cited by
133
References
105
Citations by year
2026: 4 · 2025: 3 · 2024: 5 · 2023: 9 · 2022: 5 · 2021: 6 · 2020: 8 · 2019: 12 · 2018: 14 · 2017: 12 · 2016: 8 · 2015: 17 · 2014: 12 · 2013: 12 · 2012: 6
FWCI
1.73
Type
journal article
Language
en
Open access
Locations
  • Molecular and Cellular Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Funders
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
  • Agence Nationale pour la Gestion des Déchets Radioactifs
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
insulin secretion, pancreatic beta cells, mitochondrial function, mitochondrial calcium uptake, mitochondrial matrix pH, membrane depolarization, calcium influx, insulin granule exocytosis, ATP production, nutrient sensing, type 2 diabetes
MeSH terms
Insulin Secretion, Adenosine Triphosphate, Animals, Calcium, Cell Membrane, Diabetes Mellitus, Type 2, Exocytosis, Humans, Insulin, Membrane Potentials, Mitochondria, Oxidative Phosphorylation, Insulin-Secreting Cells

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