Role of carnitine in hepatic ketogenesis.
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TLDR
The findings suggest that the increased fatty acid flux through the carnitine acyltransferase reaction brought about by glucagon excess, with or without insulin deficiency, is mediated, at least in part, by elevation in the liver carnite concentration.Abstract:
The enhancement of long-chain fatty acid oxidation and ketogenesis in the perfused rat liver, whether induced acutely by treatment of fed animals with anti-insulin serum or glucagon, or over the longer term by starvation or the induction of alloxan diabetes, was found to ba accompanied by a proportional elevation in the tissue carnitine content. Moreover, when added to the medium perfusing livers from fed rats, carnitine stimulated ketogenesis from oleic acid. The findings suggest that the increased fatty acid flux through the carnitine acyltransferase (carnitine palmitoyl-transferase; palmitoyl-CoA:L-carnitine O-palmitoyltransferase; EC 2.3.1.21) reaction brought about by glucagon excess, with or without insulin deficiency, is mediated, at least in part, by elevation in the liver carnitine concentration.read more
Citations
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Carnitine--metabolism and functions
TL;DR: The only firmly established function of carnitine is its function as a carrier of activated fatty acids and activated acetate across the inner mitochondrial membrane, and the regulation of its synthesis is still incompletely understood.
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A possible role for malonyl-CoA in the regulation of hepatic fatty acid oxidation and ketogenesis.
TL;DR: Studied on the oxidation of oleic and octanoic acids to ketone bodies were carried out in homogenates and in mitochondrial fractions of livers taken from fed and fasted rats, and malonyl-CoA inhibited ketogenesis from the former but not from the latter substrate.
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Carnitine biosynthesis in mammals.
TL;DR: This review aims to cover the current knowledge of the enzymological, molecular, metabolic and regulatory aspects of mammalian carnitine biosynthesis, with an emphasis on the human and rat.
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Acylcarnitines: Role in brain
TL;DR: Brain acylcarnitines can function in synthesizing lipids, altering and stabilizing membrane composition, modulating genes and proteins, improving mitochondrial function, increasing antioxidant activity, and enhancing cholinergic neurotransmission.
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Glucagon physiology and pathophysiology in the light of new advances.
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References
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Journal ArticleDOI
The effects of starvation and refeeding on carbohydrate and lipid metabolism in vivo and in the perfused rat liver. The relationship between fatty acid oxidation and esterification in the regulation of ketogenesis.
TL;DR: The data obtained demonstrate that surprisingly brief periods of starvation and refeeding exert dramatic effects on glucose and fatty acid metabolism in the intact animal and that generally synchronous changes occur in the ketogenic and gluconeogenic capacities of the perfused liver.
Journal ArticleDOI
Hormonal control of ketogenesis. Rapid activation of hepatic ketogenic capacity in fed rats by anti-insulin serum and glucagon.
TL;DR: The results are consistent with the possibility that the activity of carnitine acyltransferase, and thus ketogenic capacity, is subject to bihormonal control through the relative blood concentrations of insulin and glucagon, as also appears to be the case with hepatic carbohydrate metabolism.
Journal ArticleDOI
Control of Gluconeogenesis in Liver IV. DIFFERENTIAL EFFECTS OF FATTY ACIDS AND GLUCAGON ON KETOGENESIS AND GLUCONEOGENESIS IN THE PERFUSED RAT LIVER
TL;DR: It is concluded that fatty acids probably do not play a physiological role in the rapid regulation of hepatic gluc oneogenesis, and that glucagon does not stimulate gluconeogenesis by activating hepatic lipolysis.
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