BCHM 462 Lecture Notes - Lecture 2: Glycogen Phosphorylase, Phosphofructokinase 2, Gluconeogenesis

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These are my notes that conclude material for the first exam. What i don"t give in lecture, you have here: glycolysis vs. glucose secretion in liver, substrate cycle regulates [fructose-2,6-bisphosphate] two competing activites in one protein (nc 6th ed. pp. Gluconeogenesis phosphorylase will dephosphorylated: since capk is active under conditions of high epinephrine/glucagon, glycogen be phosphorylated and active ( glycogenolysis) and glycogen synthase will be and inactive ( glycogen synthesis). active being promote. Therefore, [glucose] for export to blood, since liver can"t use glucose for glycolysis for itself: effect of insulin pp2a dephosphorylates bifunctional protein to yield inactive fbpase-2 and. Fbpase-2 used instead gluconeogenesis gluconeogenesis (from work on rat and frog: citrate and pep inhibit pfk-2/activate fbpase-2 therefore [f2,6bp] Pfk-1 is deactivated and fbpase-1 is deinhibited, so glycolysis and : f6p activates pfk-2/inhibits fbpase-2 therefore [f2,6bp] Pfk-1 is activated and fbpase-1 is inhibitied, so glycolysis and : in adipose tissue, fbpase-2/pfk-2 bifunctional protein not a major player.