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Neuman, I. et al.

Neuman, Maloberti, Lisdero, Colonna, Peralta, José, Podestá,

beta-Adrenergic stimulation controls the expression of a thioesterase specific for very-long-chain fatty acids in perfused hearts.

Arachidonic acid is not freely stored in the cells. A number of different pathways for the mobilization of this compound have been proposed, including a novel mechanism that involves the release of arachidonic acid from arachidonoyl-CoA by a thioesterase with substrate specificity for very-long-chain fatty acids. In rat heart, the acyl-CoA thioesterase activity can be regulated by a mechanism that involves beta-adrenoceptors. In this paper we demonstrate that beta-adrenergic agonists also regulate the acyl-CoA thioesterase mRNA levels. Isoproterenol (10(-7)M)-a concentration known to exert physiological responses-increases in a time-dependent manner the acyl-CoA thioesterase mRNA levels, an effect blocked by a specific beta-adrenoceptor antagonist. In addition, our results show that cAMP is involved in this process. The acyl-CoA thioesterase mRNA levels are also increased by fasting, but not by di(2-ethylhexyl)phthalate, a peroxisome proliferator. These results may suggest the existence of a beta-adrenoceptor-activated regulatory pathway for arachidonic acid release in cardiac tissue.[1]

References

beta-Adrenergic stimulation controls the expression of a thioesterase specific for very-long-chain fatty acids in perfused hearts. Neuman, I., Maloberti, P., Lisdero, C., Colonna, C., Peralta, J., José, J.P., Podestá, E.J. Biochem. Biophys. Res. Commun. (2002) [Pubmed]

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