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The molecular mechanisms of inhibitory effect of androstenone on hepatic skatole metabolism in relation to boar taint

Published online by Cambridge University Press:  23 November 2017

E. Doran
Affiliation:
Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol BS40 5DU, U.K.
J. D. McGivan*
Affiliation:
Department of Biochemistry, University of Bristol, University Walk, Bristol BS8 1TK, U.K.
M.F. Whittington
Affiliation:
Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol BS40 5DU, U.K.
J. D. Wood
Affiliation:
Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol BS40 5DU, U.K.
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Extract

Boar taint is off-odours in cooked pork from uncastrated male pigs. It is caused by an excessive accumulation of skatole and androstenone in backfat. Accumulation of skatole is due to a low expression and activity of hepatic enzyme CYP2E1. The mechanism of androstenone accumulation is not clear. It could be due to low activity and expression of 3ß-hydroxysteroid dehydrogenase (HSD), an enzyme metabolising androstenone in liver. On the basis of our previous in vivo experiments with castrated animals we suggest that accumulation of skatole is regulated by androstenone. Castrated pigs manifest lower levels of skatole and androstenone and higher CYP2E1 expression. We hypothesise that high levels of androstenone inhibits CYP2E1 expression and hence, reduces the rate of hepatic skatole metabolism. The aims of the present study were (i) to investigate the expression of androstenone-metabolising enzyme HSD in liver of pigs with high and low skatole and androstenone deposition; (ii) to investigate the effect of androstenone on expression of the skatole-metabolising enzyme CYP2E1 in vitro (in cell culture).

Type
Theatre Presentations
Copyright
Copyright © The British Society of Animal Science 2005

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