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Boron, W. F., and Boulpaep, E. L. (2009). Medical Physiology. Brown, A. M. (2004). Brain glycogen health formula re-awakened. Brown, A. M., Sickmann, H. M., Fosgerau, K., Lund, T. M., Schousboe, A., Waagepetersen, H. S., et al. 2005). Astrocyte glycogen metabolism is required for neural activity during aglycemia or intense stimulation in mouse white matter. Brown, A. M., Tekkok, S. B., and Ransom, B. R. (2003). Glycogen regulation and functional role in mouse white matter. Brown, A. M., Wender, R., and Ransom, B. R. (2001a). Ionic mechanisms of aglycemic axon harm in mammalian central white matter. J. Cereb. Blood Flow Metab. Brown, A. M., Wender, R., and Ransom, B. R. (2001b). Metabolic substrates apart from glucose support axon function in central white matter. Carrard, A., Elsayed, M., Margineanu, M., Boury-Jamot, B., Fragniere, L., Meylan, E. M., et al. 2018). Peripheral administration of lactate produces antidepressant-like effects. Cataldo, A. M., and Broadwell, R. D. (1986). Cytochemical identification of cerebral glycogen and glucose-6-phosphatase exercise under regular and experimental conditions.

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Since this molecule is a potent activator of PFK-1 and inhibitor of FBPase-1, its reduction inhibits glycolysis and stimulates gluconeogenesis. Therefore, in response to glucagon, hepatic glucose production increases, serving to the liver counteract the drop in blood glucose levels. Note: like adrenaline, glucagon also promotes gluconeogenesis by growing the availability of key substrates similar to glycerol and amino acids. Insulin has the opposite effect. Insulin additionally stimulates cAMP phosphodiesterase, which degrades cAMP into AMP, further reducing PKA activity. The result's a rise in F2,6BP ranges, which inhibits gluconeogenesis and stimulates glycolysis. PFK-2 and FBPase-2 are subject to product inhibition. However, the primary regulatory factors are the extent of fructose 6-phosphate and the phosphorylation state of the bifunctional enzyme. Unlike pyruvate carboxylase and fructose-1,6-bisphosphatase, the catalytic subunit of glucose 6-phosphatase is just not regulated allosterically or by way of covalent modification. Instead, its activity is modulated on the transcriptional degree. Conditions that promote glucose production, corresponding to low blood glucose, glucagon, and glucocorticoids, stimulate the expression of the enzyme.