Cited by 95Mitochondrial Function and PathologyAdipose Tissue and MetabolismMetabolism, Diabetes, and Cancer

The DOI matches its Crossref record; 123 of the 123 references it cites were found in a registry or an index.

Mitochondrial Uncoupling: Role of Uncoupling Protein Anion Carriers and Relationship to Thermogenesis and Weight Control “The Benefits of Losing Control”

Diehl, Anna Mae, Hoek, Jan B.·1999·Journal of Bioenergetics and Biomembranes

Abstract

Uncoupling proteins, a subgroup of the mitochondrial anion transporter superfamily, have been identified in prokaryotes, plants, and mammalian cells. Evolutionary conservation of these molecules reflects their importance as regulators of two critical mitochondrial functions, i.e., ATP synthesis and the production of reactive oxygen species (ROS). Although the amino acid sequences of the three mammalian uncoupling proteins, UCP1, UCP2 and UCP3, are very similar, each homolog is the product of a unique gene and important differences have been demonstrated in their tissue-specific expression and regulation. UCP1 and UCP3 appear to be key regulators of energy expenditure, and hence, nonshivering thermogenesis, either in brown adipose tissue (UCP1) or skeletal muscle (UCP3). UCP2 is expressed more ubiquitously, although generally at low levels, in many tissues. There is conflicting evidence about its importance as a regulator of resting metabolic rate. However, evidence suggests that this homolog might modulate the mitochondrial generation of ROS in some cell types, including macrophages and hepatocytes. While the induction of various uncoupling protein homologs provides adaptive advantages, both to the organism (e.g., thermogenesis) and to individual cells (e.g., reduced ROS), increased uncoupling protein activity also increases cellular vulnerability to necrosis by compromising the mitochondrial membrane potential. This narrow "risk-benefit" margin necessitates tight control of uncoupling protein activity in order to preserve cellular viability and much remains to be learned about the regulatory mechanisms involved.

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Crossref · 10.1023/a:1005452624640

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Research works printed but not linked: 15

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Metadata

Authors
Diehl, A. M., & Hoek, J. B.
Affiliations
  • Johns Hopkins University (US)
  • Thomas Jefferson University (US)
Corresponding author
Diehl, Anna Mae
Venue
Journal of Bioenergetics and Biomembranes
Published
1999-10
Volume
31
Issue
5
Pages
493-506
ISSN
  • 0145-479X (ISSN-L)
  • 1573-6881
OpenAlex
W56406267
Cited by
95
References
122
Citations by year
2025: 1 · 2024: 2 · 2022: 1 · 2021: 1 · 2018: 7 · 2017: 4 · 2016: 1 · 2015: 3 · 2014: 5 · 2013: 2 · 2012: 4
FWCI
0.66
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Bioenergetics and Biomembranes (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
uncoupling proteins, mitochondrial uncoupling, UCP1, UCP2, UCP3, thermogenesis, brown adipose tissue, skeletal muscle, energy expenditure, weight management, reactive oxygen species, mitochondrial membrane potential, necrosis, resting metabolic rate, tissue-specific gene expression
MeSH terms
Uncoupling Protein 2, Uncoupling Protein 1, Animals, Anions, Body Weight, Carrier Proteins, Ion Channels, Membrane Proteins, Mitochondria, Proteins, Uncoupling Agents, Apoptosis, Reactive Oxygen Species, Mitochondrial Proteins, Membrane Transport Proteins

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