The Biology of Mitochondrial Uncoupling Proteins

  1. Sophie Rousset,
  2. Marie-Clotilde Alves-Guerra,
  3. Julien Mozo,
  4. Bruno Miroux,
  5. Anne-Marie Cassard-Doulcier,
  6. Frédéric Bouillaud and
  7. Daniel Ricquier
  1. From the Centre National de la Recherche Scientifique, Unité Propre de Recherche 9078, Faculté de Médecine and Institut de Recherches Necker-Enfants Malades (IRNEM), Paris, France
  1. Address correspondence and reprint requests to Dr. D. Ricquier, Faculté de Médecine, Necker-Enfants Malades, CNRS UPR 9078, 7ème étage, 75730 Paris, Cedex 15, France. E-mail: ricquier{at}necker.fr

Abstract

Uncoupling proteins (UCPs) are mitochondrial transporters present in the inner membrane of mitochondria. They are found in all mammals and in plants. They belong to the family of anion mitochondrial carriers including adenine nucleotide transporters. The term “uncoupling protein” was originally used for UCP1, which is uniquely present in mitochondria of brown adipocytes, the thermogenic cells that maintain body temperature in small rodents. In these cells, UCP1 acts as a proton carrier activated by free fatty acids and creates a shunt between complexes of the respiratory chain and ATP synthase. Activation of UCP1 enhances respiration, and the uncoupling process results in a futile cycle and dissipation of oxidation energy as heat. UCP2 is ubiquitous and highly expressed in the lymphoid system, macrophages, and pancreatic islets. UCP3 is mainly expressed in skeletal muscles. In comparison to the established uncoupling and thermogenic activities of UCP1, UCP2 and UCP3 appear to be involved in the limitation of free radical levels in cells rather than in physiological uncoupling and thermogenesis. Moreover, UCP2 is a regulator of insulin secretion and UCP3 is involved in fatty acid metabolism.

Footnotes

  • This article is based on a presentation at a symposium. The symposium and the publication of this article were made possible by an unrestricted educational grant from Les Laboratoires Servier.

    • Accepted April 2, 2003.
    • Received March 13, 2003.
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