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.
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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“Gain-of-function studies in mice where ectopic expression of UCPs mitigate diet-induced obesity support the notion that uncoupling could be sufficient (183, 184).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [184]
Citations
Cites
The Ecological Implications of Body Size
Peters, R. H. (1983) · Cambridge University Press eBooks · doi:10.1017/cbo9780511608551 · Cited by 5,757
Kopelman, P. G. (2000) · Nature · doi:10.1038/35007508 · Cited by 4,795
Size, Function, and Life History
Calder, W. A. (1984) · Medical Entomology and Zoology · Cited by 2,864
Kleiber, M. (1932) · Hilgardia · doi:10.3733/hilg.v06n11p315 · Cited by 2,222
Jaap, R. G. (1946) · Poultry Science · doi:10.3382/ps.0250096 · Cited by 2,205
Uncoupling protein-2: a novel gene linked to obesity and hyperinsulinemia
Fleury, C., Neverova, M., Collins, S., Raimbault, S., Champigny, O., Lévi-Meyrueis, C., Bouillaud, F., Seldin, M. F., Surwit, R. S., Ricquier, D., et al. (1997) · Nature Genetics · doi:10.1038/ng0397-269 · Cited by 1,630
Thermogenic mechanisms in brown fat.
Nicholls, D. G., & Locke, R. M. (1984) · Physiological Reviews · doi:10.1152/physrev.1984.64.1.1 · Cited by 1,602 · cited 14×
“The identification of UCP1 as the mediator of uncoupling followed from the observation of greater uncoupling of BAT mitochondria than of liver and heart mitochondria (77,78).”
InfluentialMice lacking mitochondrial uncoupling protein are cold-sensitive but not obese
Enerbäck, S., Jacobsson, A., Simpson, E. M., Guerra, C., Yamashita, H., Harper, M.-E., & Kozak, L. P. (1997) · Nature · doi:10.1038/387090a0 · Cited by 1,379
Sjöström, L., Rissanen, A., Andersen, T., Boldrin, M., Golay, A., Koppeschaar, H. P., & Krempf, M. (1998) · The Lancet · doi:10.1016/s0140-6736(97)11509-4 · Cited by 1,237
Field Metabolic Rate and Food Requirement Scaling in Mammals and Birds
Nagy, K. A. (1987) · Ecological Monographs · doi:10.2307/1942620 · Cited by 990
Research works printed but not linked: 7
- CazeneuzeP&LepineR.Compt Rend Soc Biol1885;101:1167–1169.
- Magne H, 1932, Studies on the action of dinitrophenol 1–2–4 (Thermol)., Ann Physiol Physicochem Biol, 8, 1
- Tainter ML, 1935, Dinitrophenol in the treatment of obesity: Final report., J Am Med Assoc, 101, 322
- Anthony DM, 2001, Obesity Regulation Energy Homeostasis Keystone Symposia., 218
- Byrom FB., 1933, Nature of myxoedema., Clin Sc, 1, 273
- Stuart JA, 2001, Obesity Regulation Energy Homeostasis Keystone Symposia., 218
- 10.1042/0264-6021:3510307 · DOI
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Rosen, E. D., & Spiegelman, B. M. (2014) · Cell · doi:10.1016/j.cell.2013.12.012 · Cited by 2,373
Brown and beige fat: Development, function and therapeutic potential
Harms, M., & Seale, P. (2013) · Nature Medicine · doi:10.1038/nm.3361 · Cited by 2,328
Mechanism of hepatic insulin resistance in non-alcoholic fatty liver disease
Samuel, V. T., Liu, Z.-X., Qu, X., Elder, B. D., Bilz, S., Befroy, D., Romanelli, A. J., & Shulman, G. I. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m313478200 · Cited by 1,322
Mitochondria as a therapeutic target for common pathologies
Murphy, M. P., & Hartley, R. C. (2018) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2018.174 · Cited by 846
Mitochondrial proton and electron leaks
Jastroch, M., Divakaruni, A. S., Mookerjee, S., Treberg, J. R., & Brand, M. D. (2010) · Essays in Biochemistry · doi:10.1042/bse0470053 · Cited by 829
Self-citation
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
- 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
- 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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