The intracellular concentration of free unbound acyl-CoA esters is tightly controlled by feedback inhibition of the acyl-CoA synthetase and is buffered by specific acyl-CoA binding proteins. Excessive increases in the concentration are expected to be prevented by conversion into acylcarnitines or by hydrolysis by acyl-CoA hydrolases. Under normal physiological conditions the free cytosolic concentration of acyl-CoA esters will be in the low nanomolar range, and it is unlikely to exceed 200 nM under the most extreme conditions. The fact that acetyl-CoA carboxylase is active during fatty acid synthesis (Ki for acyl-CoA is 5 nM) indicates strongly that the free cytosolic acyl-CoA concentration is below 5 nM under these conditions. Only a limited number of the reported experiments on the effects of acyl-CoA on cellular functions and enzymes have been carried out at low physiological concentrations in the presence of the appropriate acyl-CoA-buffering binding proteins. Re-evaluation of many of the reported effects is therefore urgently required. However, the observations that the ryanodine-senstitive Ca2+-release channel is regulated by long-chain acyl-CoA esters in the presence of a molar excess of acyl-CoA binding protein and that acetyl-CoA carboxylase, the AMP kinase kinase and the Escherichia coli transcription factor FadR are affected by low nanomolar concentrations of acyl-CoA indicate that long-chain acyl-CoA esters can act as regulatory molecules in vivo. This view is further supported by the observation that fatty acids do not repress expression of acetyl-CoA carboxylase or Δ9-desaturase in yeast deficient in acyl-CoA synthetase.
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April 1997
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Review Article| April 01 1997
Role of long-chain fatty acyl-CoA esters in the regulation of metabolism and in cell signalling
Nils Joakim FÆRGEMAN;
Nils Joakim FÆRGEMAN
1Institute of Biochemistry, Odense University, DK-5230 Odense, Denmark
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Jens KNUDSEN
Jens KNUDSEN *
1Institute of Biochemistry, Odense University, DK-5230 Odense, Denmark
*To whom correspondence should be addressed.
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Publisher: Portland Press Ltd
Online ISSN: 1470-8728
Print ISSN: 0264-6021
The Biochemical Society, London © 1997
1997
Biochem J (1997) 323 (1): 1–12.
Citation
Nils Joakim FÆRGEMAN, Jens KNUDSEN; Role of long-chain fatty acyl-CoA esters in the regulation of metabolism and in cell signalling. Biochem J 1 April 1997; 323 (1): 1–12. doi: https://doi.org/10.1042/bj3230001
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