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Cited by 250Adipose Tissue and MetabolismMitochondrial Function and PathologyPharmacology and Obesity Treatment

The DOI matches its Crossref record; 119 of the 119 references it cites were found in a registry or an index.

Mitochondrial uncoupling as a target for drug development for the treatment of obesity.

Harper, J. A., Dickinson, K., Brand, M. D.·2001·Obesity Reviews
DOI 10.1046/j.1467-789x.2001.00043.x
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Abstract

Mitochondrial proton cycling is responsible for a significant proportion of basal or standard metabolic rate, so further uncoupling of mitochondria may be a good way to increase energy expenditure and represents a good pharmacological target for the treatment of obesity. Uncoupling by 2,4-dinitrophenol has been used in this way in the past with notable success, and some of the effects of thyroid hormone treatment to induce weight loss may also be due to uncoupling. Diet can alter the pattern of phospholipid fatty acyl groups in the mitochondrial membrane, and this may be a route to uncoupling in vivo. Energy expenditure can be increased by stimulating the activity of uncoupling protein 1 (UCP1) in brown adipocytes either directly or through beta 3-adrenoceptor agonists. UCP2 in a number of tissues, UCP3 in skeletal muscle and the adenine nucleotide translocase have also been proposed as possible drug targets. Specific uncoupling of muscle or brown adipocyte mitochondria remains an attractive target for the development of antiobesity drugs.

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Crossref · 10.1046/j.1467-789x.2001.00043.x

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119 of 119 references verified0 citation errors · 0 not checkable

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Research works printed but not linked: 7

  1. CazeneuzeP&LepineR.Compt Rend Soc Biol1885;101:1167–1169.
  2. Magne H, 1932, Studies on the action of dinitrophenol 1–2–4 (Thermol)., Ann Physiol Physicochem Biol, 8, 1
  3. Tainter ML, 1935, Dinitrophenol in the treatment of obesity: Final report., J Am Med Assoc, 101, 322
  4. Anthony DM, 2001, Obesity Regulation Energy Homeostasis Keystone Symposia., 218
  5. Byrom FB., 1933, Nature of myxoedema., Clin Sc, 1, 273
  6. Stuart JA, 2001, Obesity Regulation Energy Homeostasis Keystone Symposia., 218
  7. 10.1042/0264-6021:3510307 · DOI

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Metadata

Authors
Harper, J. A., Dickinson, K., & Brand, M. D.
Affiliations
  • University of Cambridge (GB)
  • MRC Mitochondrial Biology Unit (GB)
Corresponding author
Brand, M. D.
ORCID
Brand, M. D.
Venue
Obesity Reviews
Publisher
Wiley
Published
2001-11
Volume
2
Issue
4
Pages
255-265
ISSN
  • 1467-7881 (ISSN-L)
  • 1467-789X
DOI
10.1046/j.1467-789x.2001.00043.x
OpenAlex
W1979144331
Cited by
250
References
119
Citations by year
2026: 2 · 2025: 1 · 2024: 6 · 2023: 9 · 2022: 7 · 2021: 6 · 2020: 19 · 2019: 9 · 2018: 12 · 2017: 9 · 2016: 11 · 2015: 19 · 2014: 25 · 2013: 12 · 2012: 15
FWCI
0.53
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2440 d)
Locations
  • Obesity Reviews (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Pharmacology (medical) › Pharmacology and Obesity Treatment
Keywords
mitochondrial uncoupling, obesity treatment, energy expenditure, UCP1, brown adipocytes, beta3-adrenergic agonists, UCP2, UCP3, adenine nucleotide translocase, 2,4-dinitrophenol, thyroid hormones, mitochondrial membrane phospholipids, anti-obesity drugs
MeSH terms
Uncoupling Protein 1, Basal Metabolism, Carrier Proteins, Energy Metabolism, Humans, Ion Channels, Membrane Proteins, Mitochondria, Obesity, Weight Loss, Anti-Obesity Agents, Mitochondrial Proteins

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