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Abstract
The con ve rsio n of phosphoenolpyruvate to glucose represents a reversal of part of the glycolysis sequence. It will be convenient to discuss this along with the reversal of the complete glycolysis sequence from lactic. The latter, which is called gluconeogenesis, is an essential part of the Cori cycle. The same process may be used by the body to convert pyruvate derived from deamination of alanine or serine into carbohydrates. If a large amount of lactate enters the liver it is oxidized to pyruvate which enters the mitochondria. There is part of pyruvate that it is oxidized through the citric acid cyele. However if ATP is high pyruvate dehydrogenase is blocked. If this happens, the amount of pyruvate converted to oxalacetate and malate may increase. Malate may leave the mitochondrion to be reoxidized to oxalacetate which is then converted to phosphoenolpyruvate and on to glycogeri. Gluconeogenesis in liver is strongly promoted by glucagon and catecholamines. The effects, mediated by cAMP, may inelude stimulation of fructose 1,6-bisphosphatase and inhibition of phosphofructokinase. During prolonged fasting glycogen supplies are depleted and fats become the principal fuel. Both glucose and pyruvate are in short supply. While the hydrolisis of lipids provide sorne glycerol the quantity of glucose precursors formed in this way is limited.
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