The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
The Role of the Carnitine System in Human Metabolism
Abstract
A bstract:Metabolism cycles daily between the fed and fasted states. The pathways of energy production are reversible and distinct. In the anabolic (fed) state, the liver stores glucose as glycogen, and fatty acid/triglyceride synthesis is active. In the catabolic (fasted) state, the liver becomes a glucose producer, lipogenesis is slowed, and fatty acid oxidation/ketogenesis is activated. The rate‐limiting step for the latter is vested in the carnitine/carnitine palmitoyltransferase (CPT) system, and the off/on regulator of this is malonyl CoA. The AMP‐induced protein kinase primarily determines the concentration of malonyl CoA. Four other systems have significant influence: two on fatty acid oxidation and two on lipogenesis. Peroxisome proliferator‐activated receptor γ‐1α, a master regulator of metabolism, induces hepatic gluconeogenesis and fatty acid oxidation in the catabolic phase. Deficiency of stearoyl CoA desaturase, although having no role in gluconeogenesis, powerfully induces fatty acid oxidation and weight loss despite increased food intake in rodents. Major stimulators of lipogenesis are carbohydrate‐responsive element binding protein and the Insig system. The malonyl CoA‐regulated CPT system has been firmly established in humans. The other systems have not yet been confirmed in humans, but likely are active there as well. Activation of fatty acid oxidation has considerable clinical promise for the treatment of obesity, type 2 diabetes, steatohepatitis, and lipotoxic damage to the heart.
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Cites
Cloning of adiponectin receptors that mediate antidiabetic metabolic effects
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“The sequence is (1) activation of AMP kinase kinase (AMPKK) by phosphorylation or binding of fatty acyl CoA, (2) activation of AMPK by AMPKK phosphorylation, (3) inhibition of acetyl CoA carboxylase (ACC) by AMPKmediated phosphorylation, and (4) activation of malonyl CoA decarboxylase (MCD) by AMPK phosphorylation.”
BackgroundSelf-citationPeroxisome-Proliferator-Activated Receptor δ Activates Fat Metabolism to Prevent Obesity
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Peroxisome proliferator–activated receptor γ coactivator-1 promotes cardiac mitochondrial biogenesis
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Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2
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Minireview: Malonyl CoA, AMP-Activated Protein Kinase, and Adiposity
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PGC-1β in the Regulation of Hepatic Glucose and Energy Metabolism
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Cited by
Berger, M. M., Shenkin, A., Schweinlin, A., Amrein, K., Augsburger, M., Biesalski, H.-K., Bischoff, S. C., Casaer, M. P., Gundogan, K., Lepp, H.-L., et al. (2022) · Clinical Nutrition · doi:10.1016/j.clnu.2022.02.015 · Cited by 615
Regulation of autophagy by cytosolic acetyl-coenzyme A
Mariño, G., Pietrocola, F., Eisenberg, T., Kong, Y., Malik, S. A., Andryushkova, A., Schroeder, S., Pendl, T., Harger, A., Niso-Santano, M., et al. (2014) · Molecular Cell · doi:10.1016/j.molcel.2014.01.016 · Cited by 500
Jones, L. L., McDonald, D. A., & Borum, P. R. (2010) · Progress in Lipid Research · doi:10.1016/j.plipres.2009.08.004 · Cited by 454
Dynamics of the Cellular Metabolome during Human Cytomegalovirus Infection
Munger, J., Bajad, S. U., Coller, H. A., Shenk, T., & Rabinowitz, J. D. (2006) · PLoS Pathogens · doi:10.1371/journal.ppat.0020132 · Cited by 417
Proteolytic and lipolytic responses to starvation
Finn, P. F., & Dice, J. F. (2006) · Nutrition · doi:10.1016/j.nut.2006.04.008 · Cited by 321
Metadata
- Authors
- FOSTER, D. W.
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2004-11
- Volume
- 1033
- Issue
- 1
- Pages
- 1-16
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W2043605177
- Cited by
- 230
- References
- 11
- FWCI
- 2.84
- Type
- journal article
- Language
- en
- Open access
- closed
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