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This research aims to explore the reversible inactivation effect of noradrenaline on fatty acyl-CoA synthetase in rat adipocytes.

February 15, 1985Biochemical JournalOpen Access

Reversible inactivation by noradrenaline of long-chain fatty acyl-CoA synthetase in rat adipocytes

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This research aims to explore the reversible inactivation effect of noradrenaline on fatty acyl-CoA synthetase in rat adipocytes.
Investigated effects of noradrenaline, corticotropin, and glucagon on fatty acyl-CoA synthetase activity in rat adipocytes.
Introduced a novel fluorescence assay for measuring fatty acyl-CoA synthetase activity.
Tested enzyme activity post-treatment with insulin and propranolol to assess reversibility.
Noradrenaline caused a significant decrease in fatty acyl-CoA synthetase activity over a wide concentration range.
The reversible effect of noradrenaline persisted despite various treatments, including microsomal fractionation and Triton X-100 exposure.
Insulin and propranolol effectively reversed the inactivation of fatty acyl-CoA synthetase by noradrenaline.

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Randomized trial investigates noradrenaline's impact on fatty acyl-CoA synthetase in rat adipocytes, suggesting significant metabolic regulation.

Hall et al. (1985) studied this question.

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Randomized trial investigates noradrenaline's impact on fatty acyl-CoA synthetase in rat adipocytes, suggesting significant metabolic regulation.