A sudden decrease in blood glucose will cause convulsions, as in insulin over- dose, owing to the immediate dependence of the brain Figure 19–3. Control of glycolysis and gluconeoge- nesis in the liver by fructose 2,6-bisphosphate and the bifunctional enzyme PFK-2/F-2,6-Pase (6-phospho- fructo-2-kinase/fructose-2,6-bisphosphatase). (PFK-1, phosphofructokinase-1 [6-phosphofructo-1-kinase];F-1,6-Pase, fructose-1,6-bisphosphatase. Arrows with wavy shafts indicate allosteric effects.)fructose-1,6-bisphosphatase. When glucose is short, glucagon stimulates the production of cAMP, activat- ing cAMP-dependent protein kinase, which in turn in- activates phosphofructokinase-2 and activates fructose 2,6-bisphosphatase by phosphorylation. Therefore, glu- coneogenesis is stimulated by a decrease in the concen- tration of fructose 2,6-bisphosphate, which deactivates phosphofructokinase-1 and deinhibits fructose-1,6-bis- phosphatase. This mechanism also ensures that glu- cagon stimulation of glycogenolysis in liver results in glucose release rather than glycolysis.
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