Effects of adrenaline on ketogenesis from long- and medium-chain fatty acids in starved rats
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1. Injection of adrenaline into 24 h-starved rats caused a 69% decrease in blood [ketone-body] (3-hydroxybutyrate plus acetoacetate), accompanied by a decreased [3-hydroxybutyrate]/[acetoacetate] ratio. Blood [glucose] and [lactate] increased, but [alanine] was unchanged. 2. Adrenaline also decreased [ketone-body] after intragastric feeding of both long- and medium-chain triacylglycerol. The latter decrease was observed after suppression of lipolysis with 5-methylpyrazole-3-carboxylic acid, indicating that the antiketogenic action of adrenaline was not dependent on the chain length of the precursor fatty acid. 3. The actions of adrenaline to decrease blood [ketone-body] and to increase blood [glucose] were not observed after administration of 3-mercaptopicolinate, an inhibitor of gluconeogenesis. This suggests that these effects of the hormone are related. 4. The possible clinical significance of the results is discussed with reference to the restricted ketosis often observed after surgical or orthopaedic injury.Keywords:
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1. The aim of this study was to determine the effect of a constant infusion of glucose on the ketosis that is observed when dairy cows are deprived of food in early lactation. 2. Cows in early lactation were first deprived of food for 4 days (96h) to induce a 'fasting ketosis'. Glucose was then infused intravenously at a constant rate of 0.75 g/min for 48h while deprivation of food was maintained. At the end of this 48 h period, blood and liver ketone-body concentrations had decreased to values well below those found in healthy fed cows. 3. On the assumption that the anti-ketogenic effect of glucose was mainly due to suppression of hepatic ketogenesis, it was concluded that two anti-ketogenic mechanisms had been identified. These were (a) a decrease in the availability of free fatty acids for hepatic oxidation, and (b) anti-ketogenic changes within the liver itself. 4. These latter anti-ketogenic changes were twofold. The first was a major increase in the hepatic concentrations of citrate and 2-oxoglutarate. The second was an increase in the degree of oxidation of the hepatic cytosol. It was proposed that both these intrahepatic changes might indicate an augmentation of the quantity of oxaloacetate available for condensation with acetyl-CoA derived from fat oxidation. 5. Hepatic glycerol 1-phosphate concentration fell substantially after glucose infusion. 6. Glucose infusion into fed cows produced qualitatively similar effects to those observed in the unfed cows. However, blood and liver ketone-body concentrations were not decreased to the same extent in the fed cows as in the unfed cows.
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It has been recently shown that nutritional ketosis is effective against seizure disorders and various acute/chronic neurological disorders. Physiologically, glucose is the primary metabolic fuel for cells. However, many neurodegenerative disorders have been associated with impaired glucose transport/metabolism and with mitochondrial dysfunction, such as Alzheimer’s/Parkinson’s disease, general seizure disorders, and traumatic brain injury. Ketone bodies and tricarboxylic acid cycle intermediates represent alternative fuels for the brain and can bypass the rate- limiting steps associated with impaired neuronal glucose metabolism. Therefore, therapeutic ketosis can be considered as a metabolic therapy by providing alternative energy substrates. It has been estimated that the brain derives over 60% of its total energy from ketones when glucose availability is limited. In fact, after prolonged periods of fasting or ketogenic diet (KD), the body utilizes energy obtained from free fatty acids (FFAs) released from adipose tissue. Because the brain is unable to derive significant energy from FFAs, hepatic ketogenesis converts FFAs into ketone bodies-hydroxybutyrate (BHB) and acetoacetate (AcAc)-while a percentage of AcAc spontaneously decarboxylates to acetone. Large quantities of ketone bodies accumulate in the blood through this mechanism. This represents a state.
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Ketonemia can be a physiological response to a reduction in dietary intake. It also may occur when energy demands exceed the energy intake. Normally, alimentary ketogenesis is the major source of ketone bodies in ruminants. During ketonemia there is increased hepatic ketone body production. During physiological ketosis, the mobilization of free fatty acids is inadequate to support a high rate of hepatic ketogenesis. However, during clinical ketosis, the hormonal status (low insulin, high glucagon/insulin ratio) in combination with hypoglycemia promotes excessive lipid mobilization and a greater hepatic removal of fatty acids and switches the liver to a higher rate of ketogenesis. The low insulin, furthermore, can impair maximal ketone body utilization, thus exacerbating the hyperketonemia.
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Ketone bodies are energetically efficient metabolic substrates, which are synthesised from lipids during prolonged caloric deprivation. Once considered a simple metabolite to fuel the brain during starvation, ketone bodies are now recognised as having pleiotropic effects on metabolism, including modulating the availability and catabolism of other substrates. The combination of improved energetics and fuel sparing observed during ketosis is pivotal to maintaining energy homeostasis during starvation or fasting. Harnessing these actions may also offer a method to enhance human endurance. Owing to the necessity of depleting carbohydrate stores to induce ketogenesis, exercising during an endogenous ketosis is unlikely to be advantageous. In contrast, the delivery of exogenous ketones creates a novel physiological state, where high circulating ketone concentrations and replete carbohydrate stores are present. Here, we discuss the current understanding of how exogenous ketosis may mimic advantageous aspects of starvation physiology and in doing so, be used to enhance human exercise endurance performance.
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Summary Blood chemical values, including ketone bodies, were measured in 25 cows with abomasal displacement (displacement group), 16 cows with primary ketosis (ketosis group), and nine normal controls to investigate the pathophysiology of abomasal displacement. Increases in aspartate aminotransferase, γ‐glutamyl transpeptidase, non‐esterified fatty acid (NEFA), and ketone bodies (3‐hydroxybutyric acid and acetoacetic acid) were observed in the displacement and ketosis groups. Total cholesterol increased significantly in the ketosis group but decreased in the displacement group. Glucose was significantly low and reversely correlated to ketone bodies in the ketosis group but was not low and was not correlated with ketone bodies in the displacement group. While NEFA was correlated to ketone bodies in the ketosis group, it was not in the displacement group. A correlation between the values of acetoacetic acid and 3‐hydroxybutyric acid was seen in both the ketosis and displacement groups. The fact that blood chemical values in ketosis cows were clearly different from those in displacement cows suggests that the biochemical mechanism of ketogenesis is different between these two groups.
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It has been recently shown that nutritional ketosis is effective against seizure disorders and various acute/chronic neurological disorders. Physiologically, glucose is the primary metabolic fuel for cells. However, many neurodegenerative disorders have been associated with impaired glucose transport/metabolism and with mitochondrial dysfunction, such as Alzheimer’s/Parkinson’s disease, general seizure disorders, and traumatic brain injury. Ketone bodies and tricarboxylic acid cycle intermediates represent alternative fuels for the brain and can bypass the ratelimiting steps associated with impaired neuronal glucose metabolism. Therefore, therapeutic ketosis can be considered as a metabolic therapy by providing alternative energy substrates. It has been estimated that the brain derives over 60% of its total energy from ketones when glucose availability is limited. In fact, after prolonged periods of fasting or ketogenic diet (KD), the body utilizes energy obtained from free fatty acids (FFAs) released from adipose tissue. Because the brain is unable to derive significant energy from FFAs, hepatic ketogenesis converts FFAs into ketone bodies-hydroxybutyrate (BHB) and acetoacetate (AcAc)-while a percentage of AcAc spontaneously decarboxylates to acetone. Large quantities.
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Non-diabetic ketosis was produced experimentally in fasted pregnant guinea pigs. Total CO 2 output of ketotic animals was less than that of appropriate controls but there was no impairment in the conversion of acetate-1-C 14 to C 14 O 2 . Sterol synthesis increased in ketotic animals while fatty acid synthesis, particularly in carcass, showed the expected decrease. Ketosis was accompanied by an increase in plasma total fatty acids and in the fatty acid concentration of liver. The experimental findings support the hypothesis that ketosis is a manifestation of increased ketogenesis rather than impaired utilization of ketone bodies.
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