Fatty acid oxidation and esterification in isolated rat hepatocytes: regulation by dibutyryl adenosine 3′,5′-cyclic monophosphate

Isolated rat hepatocytes rapidly utilized [14C] palmitate and, in particular, synthesized large amounts of neutral lipids from palmitate. Incorporation into cellular lipids occurred at a linear rate proportional to the medium concentration of fatty acids. Oxidation of [14C]palmitate to CO2 increased...

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Main Authors: Charles J. Homcy, Simeon Margolis
Format: Article
Language:English
Published: Elsevier 1973-11-01
Series:Journal of Lipid Research
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520368504
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author Charles J. Homcy
Simeon Margolis
author_facet Charles J. Homcy
Simeon Margolis
author_sort Charles J. Homcy
collection DOAJ
description Isolated rat hepatocytes rapidly utilized [14C] palmitate and, in particular, synthesized large amounts of neutral lipids from palmitate. Incorporation into cellular lipids occurred at a linear rate proportional to the medium concentration of fatty acids. Oxidation of [14C]palmitate to CO2 increased with time and was much slower than palmitate esterification. Since [14C]acetate and [14C]glucose were oxidized to CO2 at a linear rate, the lag in fatty acid oxidation to CO2 did not involve enzymatic steps subsequent to acetate formation. The relative contribution of palmitate to esterification and to CO2 formation depended upon the molar ratio of palmitate to albumin (ν) and the length of incubation. Dibutyryl cyclic AMP (1 mM) reduced the oxidation of palmitate and acetate to CO2 by about 50 and 90%, respectively, but did not alter palmitate esterification. However, equivalent concentrations of sodium butyrate produced similar decreases in CO2 formation. Dibutyryl cyclic AMP (1 mM) also stimulated palmitate oxidation to water-soluble products, principally ketone bodies, by 50–100%. Sodium butyrate exerted no effect, while monobutyryl cyclic AMP and cyclic AMP both stimulated this pathway significantly. These results indicate that both v and dibutyryl cyclic AMP regulate the metabolism of fatty acids by isolated hepatocytes and suggest that hormonal stimulation of adenyl cyclase controls hepatic lipid metabolism.
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spelling doaj.art-77ecc631d8184a62925c5932fb27fd962022-12-21T21:30:22ZengElsevierJournal of Lipid Research0022-22751973-11-01146678687Fatty acid oxidation and esterification in isolated rat hepatocytes: regulation by dibutyryl adenosine 3′,5′-cyclic monophosphateCharles J. Homcy0Simeon Margolis1Clayton Laboratories, Department of Medicine, and Department of Physiological Chemistry, The Johns Hopkins University, Baltimore, Maryland 21205Clayton Laboratories, Department of Medicine, and Department of Physiological Chemistry, The Johns Hopkins University, Baltimore, Maryland 21205Isolated rat hepatocytes rapidly utilized [14C] palmitate and, in particular, synthesized large amounts of neutral lipids from palmitate. Incorporation into cellular lipids occurred at a linear rate proportional to the medium concentration of fatty acids. Oxidation of [14C]palmitate to CO2 increased with time and was much slower than palmitate esterification. Since [14C]acetate and [14C]glucose were oxidized to CO2 at a linear rate, the lag in fatty acid oxidation to CO2 did not involve enzymatic steps subsequent to acetate formation. The relative contribution of palmitate to esterification and to CO2 formation depended upon the molar ratio of palmitate to albumin (ν) and the length of incubation. Dibutyryl cyclic AMP (1 mM) reduced the oxidation of palmitate and acetate to CO2 by about 50 and 90%, respectively, but did not alter palmitate esterification. However, equivalent concentrations of sodium butyrate produced similar decreases in CO2 formation. Dibutyryl cyclic AMP (1 mM) also stimulated palmitate oxidation to water-soluble products, principally ketone bodies, by 50–100%. Sodium butyrate exerted no effect, while monobutyryl cyclic AMP and cyclic AMP both stimulated this pathway significantly. These results indicate that both v and dibutyryl cyclic AMP regulate the metabolism of fatty acids by isolated hepatocytes and suggest that hormonal stimulation of adenyl cyclase controls hepatic lipid metabolism.http://www.sciencedirect.com/science/article/pii/S0022227520368504acetate oxidationfatty acid concentrationsbutyrateglucose oxidation
spellingShingle Charles J. Homcy
Simeon Margolis
Fatty acid oxidation and esterification in isolated rat hepatocytes: regulation by dibutyryl adenosine 3′,5′-cyclic monophosphate
Journal of Lipid Research
acetate oxidation
fatty acid concentrations
butyrate
glucose oxidation
title Fatty acid oxidation and esterification in isolated rat hepatocytes: regulation by dibutyryl adenosine 3′,5′-cyclic monophosphate
title_full Fatty acid oxidation and esterification in isolated rat hepatocytes: regulation by dibutyryl adenosine 3′,5′-cyclic monophosphate
title_fullStr Fatty acid oxidation and esterification in isolated rat hepatocytes: regulation by dibutyryl adenosine 3′,5′-cyclic monophosphate
title_full_unstemmed Fatty acid oxidation and esterification in isolated rat hepatocytes: regulation by dibutyryl adenosine 3′,5′-cyclic monophosphate
title_short Fatty acid oxidation and esterification in isolated rat hepatocytes: regulation by dibutyryl adenosine 3′,5′-cyclic monophosphate
title_sort fatty acid oxidation and esterification in isolated rat hepatocytes regulation by dibutyryl adenosine 3 5 cyclic monophosphate
topic acetate oxidation
fatty acid concentrations
butyrate
glucose oxidation
url http://www.sciencedirect.com/science/article/pii/S0022227520368504
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AT simeonmargolis fattyacidoxidationandesterificationinisolatedrathepatocytesregulationbydibutyryladenosine35cyclicmonophosphate