Cited by 209Mitochondrial Function and PathologyMetabolism, Diabetes, and CancerAutophagy in Disease and Therapy

Uncoupling protein-2 controls proliferation by promoting fatty acid oxidation and limiting glycolysis-derived pyruvate utilization

Pecqueur, Claire, Bui, Thi, Gelly, Chantal, Hauchard, Julie, Barbot, Céline, Bouillaud, Frederic, Ricquier, Daniel, Miroux, Bruno +1 more·2008·The FASEB Journal

Abstract

Uncoupling protein‐2 (UCP2) belongs to the mitochondrial carrier family and has been thought to be involved in suppressing mitochondrial ROS production through uncoupling mitochondrial respiration from ATP synthesis. However, we show here that loss of function of UCP2 does not result in a significant increase in ROS production or an increased propensity for cells to undergo senescence in culture. Instead, Ucp2—/— cells display enhanced proliferation associated with a metabolic switch from fatty acid oxidation to glucose metabolism. This metabolic switch requires the unrestricted availability of glucose, and Ucp2— /— cells more readily activate autophagy than wild‐type cells when deprived of glucose. Altogether, these results suggest that UCP2 promotes mitochondrial fatty acid oxidation while limiting mitochondrial catabolism of pyruvate. The persistence of fatty acid catabolism in Ucp2+/ + cells during a proliferative response correlates with reduced cell proliferation and enhances resistance to glucose starvation‐induced autophagy.— Pecqueur C., Bui, T., Gelly, C., Hauchard, J., Barbot, C., Bouillaud, F., Ricquier, D., Miroux, B., Thompson C. B. Uncoupling protein‐2 controls proliferation by promoting fatty acid oxidation and limiting glycolysis‐derived pyruvate utilization. FASEB J. 22, 9–18 (2008)

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Crossref · 10.1096/fj.07-8945com

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  • The critical role of UCP2 in promoting aerobic glycolysis and inhibiting oxidative phosphorylation has been established from multiple experimental models.

    “the critical role of UCP2 (uncoupling protein 2) in promoting aerobic glycolysis and inhibiting oxidative phosphorylation has been established from multiple experimental models (Pecqueur et al., 2008; Samudio et al., 2008; Bouillaud, 2009; Zhang et al., 2011).”

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Authors
Pecqueur, C., Bui, T., Gelly, C., Hauchard, J., Barbot, C., Bouillaud, F., Ricquier, D., Miroux, B., & Thompson, C. B.
Affiliations
  • Université Paris Descartes (FR)
  • Biomedical Research Building II/III Philadelphia Pennsylvania USA
  • Université Paris Descartes Faculté de Médecine site Necker Paris France
Venue
The FASEB Journal
Publisher
Wiley
Published
2007-09-13
Volume
22
Issue
1
Pages
9-18
ISSN
  • 0892-6638 (ISSN-L)
  • 1530-6860
OpenAlex
W2034872735
Cited by
209
References
42
Citations by year
2026: 1 · 2025: 5 · 2024: 9 · 2023: 14 · 2022: 15 · 2021: 14 · 2020: 9 · 2019: 11 · 2018: 10 · 2017: 12 · 2016: 11 · 2015: 16 · 2014: 17 · 2013: 9 · 2012: 11
FWCI
4.37
Type
journal article
Language
en
Open access
closed
Locations
  • The FASEB Journal (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Funders
  • European Commission (ECFP6)
  • National Institutes of Health
Topics
  • 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
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
UCP2, cell proliferation, fatty acid oxidation, pyruvate utilization, glycolysis, glucose metabolism, metabolic switch, autophagy, glucose deprivation, mitochondrial reactive oxygen species, cellular senescence, mitochondrial respiration
MeSH terms
Uncoupling Protein 2, Animals, Cells, Cultured, Cricetulus, Fatty Acids, Glycolysis, Cricetinae, Ion Channels, Oxidation-Reduction, CHO Cells, Mice, Knockout, Pyruvic Acid, Mitochondrial Proteins, Cell Proliferation, Mice

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