The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Minireview: Malonyl CoA, AMP-Activated Protein Kinase, and Adiposity
Abstract
An increasing body of evidence has linked AMP-activated protein kinase (AMPK) and malonyl coenzyme A (CoA) to the regulation of energy balance. Thus, factors that activate AMPK and decrease the concentration of malonyl CoA in peripheral tissues, such as exercise, decrease triglyceride accumulation in the adipocyte and other cells. The data reviewed here suggest that this is related to the fact that these factors concurrently increase fatty acid oxidation, decrease the esterification of fatty acids to form glycerolipids, and, by mechanisms still unknown, increase energy expenditure. Malonyl CoA contributes to these events because it is an allosteric inhibitor of carnitine palmitoyltransferase, the enzyme that controls the transfer of long-chain fatty acyl CoA from the cytosol to the mitochondria, where they are oxidized. AMPK activation in turn increases fatty acid oxidation (by effects on enzymes that govern malonyl CoA synthesis and possibly its degradation) and inhibits triglyceride synthesis. It also increases the expression of uncoupling proteins and the transcriptional regulator peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC1alpha), which could possibly increase energy expenditure. Recent studies suggest that the ability of leptin, adiponectin, 5'-aminoimidazole 4-carboxamide riboside (AICAR), adrenergic agonists, and metformin to diminish adiposity may be mediated, at least in part, by AMPK activation in peripheral tissues. In addition, preliminary studies suggest that malonyl CoA and AMPK take part in fuel-sensing and signaling mechanisms in the hypothalamus that could regulate food intake and energy expenditure.
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“While these data suggest a potential use of these compounds in improving skeletal muscle function and increasing energy expenditure, the safety issue of using AICAR or other drugs targeting AMPK needs to be considered 162.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [162]
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Cites
Central nervous system control of food intake
Schwartz, M. W., Woods, S. C., Porte, D., Seeley, R. J., & Baskin, D. G. (2000) · Nature · doi:10.1038/35007534 · Cited by 6,451
Role of AMP-Activated Protein Kinase in Mechanism of Metformin Action
Zhou, G., Myers, R., Li, Y., Chen, Y., Shen, X., Fenyk-Melody, J., Wu, M., Ventre, J., Doebber, T., Fujii, N., et al. (2001) · Journal of Clinical Investigation · doi:10.1172/jci13505 · Cited by 5,652
Leptin and the regulation of body weight in mammals
Friedman, J. M., & Halaas, J. L. (1998) · Nature · doi:10.1038/27376 · Cited by 5,405
Yamauchi, T., Kamon, J., Minokoshi, Y., Ito, Y., Waki, H., Uchida, S., Yamashita, S., Noda, M., Kita, S., Ueki, K., et al. (2002) · Nature Medicine · doi:10.1038/nm788 · Cited by 4,238
Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"?
Neel, J. V. (1962) · Europe PMC (PubMed Central) · Cited by 3,172
Obesity and the regulation of energy balance
Spiegelman, B. M., & Flier, J. S. (2001) · Cell · doi:10.1016/s0092-8674(01)00240-9 · Cited by 2,398
Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"?
(1962) · PubMed Central · Cited by 2,182
Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase
Minokoshi, Y., Kim, Y.-B., Peroni, O. D., Fryer, L. G. D., Müller, C., Carling, D., & Kahn, B. B. (2002) · Nature · doi:10.1038/415339a · Cited by 2,053
Fruebis, J., Tsao, T., Javorschi, S., Ebbets-Reed, D., Erickson, M., Yen, F. T., Bihain, B. E., & Lodish, H. F. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.98.4.2005 · Cited by 2,007
The Mitochondrial Carnitine Palmitoyltransferase System — From Concept to Molecular Analysis
McGarry, J. D., & Brown, N. F. (1997) · European Journal of Biochemistry · doi:10.1111/j.1432-1033.1997.00001.x · Cited by 1,616 · cited 2×
“Malonyl CoA is both an intermediate in the de novo synthesis of long-chain fatty acids and an inhibitor of carnitine palmitoyltransferase (CPT1), the enzyme that controls the transfer of long-chain fatty acyl CoA into mitochondria (7) (Fig.”
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Oxidative metabolism and PGC-1β attenuate macrophage-mediated inflammation
Vats, D., Mukundan, L., Odegaard, J. I., Zhang, L., Smith, K. L., Morel, C. R., Greaves, D. R., Murray, P. J., & Chawla, A. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.05.011 · Cited by 1,369
AMPK: An Emerging Drug Target for Diabetes and the Metabolic Syndrome
Zhang, B. B., Zhou, G., & Li, C. (2009) · Cell Metabolism · doi:10.1016/j.cmet.2009.03.012 · Cited by 1,042
Cool, B. L., Zinker, B. A., Chiou, W. J. H., Kifle, L., Cao, N., Perham, M., Dickinson, R., Adler, A. L., Gagné, G. D., Iyengar, R., et al. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.05.005 · Cited by 939
Yajnik, C. S., Deshpande, S. S., Jackson, A. A., Refsum, H., Rao, S., Fisher, D. J., Bhat, D., Naik, S. S., Coyaji, K., Joglekar, C. V., et al. (2007) · Diabetologia · doi:10.1007/s00125-007-0793-y · Cited by 789
AMP-activated Protein Kinase Plays a Role in the Control of Food Intake
Andersson-Hall, U. K., Filipsson, K., Abbott, C. R., Woods, A., Smith, K. L., Bloom, S. R., Carling, D., & Small, C. J. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.c300557200 · Cited by 777
Metadata
- Authors
- Ruderman, N. B., Saha, A. K., & Kraegen, E. W.
- Affiliations
- Boston University (US)
- Garvan Institute of Medical Research (AU)
- Corresponding author
- Ruderman, Neil B.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2003-12
- Volume
- 144
- Issue
- 12
- Pages
- 5166-5171
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2055061083
- Cited by
- 266
- References
- 54
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 5 · 2022: 8 · 2021: 10 · 2020: 5 · 2019: 10 · 2018: 7 · 2017: 6 · 2016: 8 · 2015: 12 · 2014: 11 · 2013: 8 · 2012: 26
- FWCI
- 7.01
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01dk019514-35)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-19514)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- malonyl-CoA, AMPK, adiposity, energy balance, fatty acid oxidation, carnitine palmitoyltransferase, triglyceride synthesis, uncoupling proteins, PGC-1α, leptin, adiponectin, AICAR, metformin, sympathomimetic drugs, food intake regulation, energy expenditure
- MeSH terms
- Adipose Tissue, Animals, Humans, Malonyl Coenzyme A, Multienzyme Complexes, Obesity, Protein Serine-Threonine Kinases, AMP-Activated Protein Kinases
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