PMID: 648Sep 1, 1975

The influence of cortisol on the enzymes of fatty acid synthesis in developing mammalian lung and brain

Pediatric Research
I GrossJ B Warshaw

Abstract

Administration of cortisol to fetal rabbits resulted in a 42% inhibition of pulmonary de novo fatty acid synthesis from acetyl coenzyme A (CoA) (P = less than 0.025). This was associated with inhibition of acetyl-CoA carboxylase (EC. 6.4.1.2.) activity (P = less than 0.01) and a tendency towards decreased activity of fatty acid synthetase. There was no effect on pulmonary microsomal fatty acid elongation activity. Light and electron microscopic examination of the apex of the right lung of control and cortisol-treated animals revealed changes consistent with accelerated lung maturation in the treated animals. The in vitro activities of acetyl-CoA carboxylase and fatty acid synthetase were similar in rabbit lung and thus acetyl-CoA carboxylase activity does not appear to be rate limiting for de novo fatty acid synthesis in lung. No significant change in the activity of enzymes associated with de novo fatty acid synthesis of microsomal fatty acid elongation was found in fetal brain after cortisol exposure. However, in a parallel study on fatty acid synthesis in fetal liver, cortisol administration resulted in a 30% increase in fatty acid synthetase activity (P less than 0.025). The finding of cortisol-induced inhibition of de novo...Continue Reading

Related Concepts

Acetyl-CoA Carboxylase
Acetyl Coenzyme A
Brain
CoASH
Saturated Fat
Fetal Structures
Hydrocortisone, (9 beta,10 alpha,11 alpha)-Isomer
Ligase
Liver
Lung

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