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All-trans-retinoic acid inhibits retinol esterification by acyl-CoA: retinol acyltransferase (EC 2.3.1.76) from rat and human small intestinal mucosa

Published online by Cambridge University Press:  09 March 2007

Müller Hanne  and
Kaare R. Norum
Müller Hanne
Affiliation:
Institute for Nutrition Research, University of Oslo, Oslo, Norway
Kaare R. Norum
Affiliation:
Institute for Nutrition Research, University of Oslo, Oslo, Norway
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Abstract

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1. Formation of retinyl esters catalyzed by acyl-CoA: retinol acyltransferase (ARAT; retinol fatty- acyltransferase; EC 2.3.1.76) from intestinal mucosa has been studied in vitro in the presence of all-trans-retinoic acid.

2. The incubation system contained microsomal preparations from the tissue tested, radioactive retinol and palmitoyl-CoA. The product formed was separated from the substrates by chromatography on alumina columns.

3. All-trans-retinoic acid inhibited ARAT both from rat and human intestinal mucosa.

4. Inhibition occurred instantly. At a concentration of retinol of 80, μM, a 50% inhibition was obtained with 50 μM- retinoic acid.

5. The inhibition of ARAT by retinoic acid may be of importance for normal retinol absorption in patients receiving retinoid therapy.

Type
Papers of direct relevance to Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 55 , Issue 1 , January 1986 , pp. 37 - 41
Copyright
Copyright © The Nutrition Society 1986

References

REFERENCES

Goodman, D. S. (1984). New England Journal of Medicine 310, 1023–1031.Google Scholar
Harrison, E. H., Smith, J. E. & Goodman, D. S. (1979). Journal of Lipid Research 20, 760–771.CrossRefGoogle Scholar
Helgerud, P., Petersen, L. B. & Norum, K. R. (1982). Journal of Lipid Research 23, 609–618.CrossRefGoogle Scholar
Helgerud, P., Petersen, L. B. & Norum, K. R. (1983). Journal of Clinical Investigation 71, 747–753.CrossRefGoogle Scholar
Helgerud, P., Saarem, K. & Norum, K. R. (1981). Journal of Lipid Research 22, 271–277.CrossRefGoogle Scholar
Huang, H. S. & Goodman, D. S. (1965). Journal of Biological Chemistry 240, 2839–2844.CrossRefGoogle Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). Journal of Biological Chemistry 193, 265–275.CrossRefGoogle Scholar
Moon, R. C. & Itri, L. M. (1984). In The Retinoids, vol. 2, pp. 327–371 [Sporn, M. B., Roberts, A. B. and Goodman, D. S., editors]. London: Academic Press.CrossRefGoogle Scholar
Norum, K. R., Helgerud, P. & Lilljeqvist, A. C. (1981). Scandinavian Journal of Gustroenterology 16, 401–410.CrossRefGoogle Scholar
Norum, K. R., Helgerud, P., Petersen, L. B., Groot, P. H. E. & De Jonge, H. R. (1983). Biochimica et Biophysica Acta 751, 153–161.CrossRefGoogle Scholar
Peck, G. L. (1984). In The Retinoids vol. 2, pp. 391–411 [Sporn, M. B., Roberts, A. B. and Goodman, D. S., editors] London: Academic Press.CrossRefGoogle Scholar
Rasmussen, M., Petersen, L. B. & Norum, K. R. (1984). British Journal of Nutrition 51, 245–253.CrossRefGoogle Scholar