Dephosphorylation glycogen synthesis

Glycogen synthase, like phosphorylase, exists in both an active and a relatively inactive form and, like phosphorylase, is subject to phosphorylation/dephosphorylation. Glycogen synthesis and breakdown are reciprocally controlled and the many different hormones and neuronal... 

Glucagon stimulation of liver cells in particular leads to phosphorylation of regulatory enzymes whereas insulin has the opposite effect. So, after a meal, we would expect glycolysis and glycogen synthesis to operate very efficiently so the control enzymes will be dephosphorylated. 

Since the enzyme glycogen synthase catalyses the rate-limiting step in glycogen synthesis, it is the activity of this enzyme that must be increased as the blood glucose concentration increases. This is achieved via an interconversion cycle (i.e. reversible phosphorylation). A protein kinase phosphorylates it, which inactivates the enzyme, whereas a protein phosphatase dephosphorylates it, which... 

Fig. 7.21. Activation of glycogen-bound protein phosphatase I by insulin. Insulin has a stimulating effect on glycogen synthesis by initiating the dephosphorylation and activation of glycogen synthase and the dephosphorylation and inhibition of glycogen phosphorylase. Both enzymes (substrate S in the figure) are dephosphorylated by protein phosphatase PPIG. Insulin mediates the activation of a protein kinase (insulin-sensitive protein kinase) within an insulin-stimulated signal pathway, which phosphorylates and thus activates protein phosphatase PPIG at the PI site.

Phosphofructo-2-kinase Enzymes of glycogen synthesis Dephosphorylation... 

In vitro, GH has many effects on adipose tissue and cells, including stimulation of lipolysis and actions on glucose utilization [89,90]. Short-term effects in vitro are mainly insulin-like (increased utilization of glucose and amino acids, glycogen synthesis, antilipolytic actions, etc.) and may be mediated by mechanisms similar to those of insulin, including dephosphorylation of hormone-sensitive lipase [91]. In the longer term adipose tissue and cells in vitro become refractory to the insulinlike effects of GH, and counter-insulin effects predominate and reflect the main actions seen in vivo. Receptors for GH have been identified in adipose tissue [90,92]. 

There must be a way to shut down the high-gain system of glycogen breakdown quickly to prevent the wasteful depletion of glycogen after energy needs have been met. Indeed, another cascade leads to the dephosphorylation and inactivation of phosphorylase kinase and glycogen phosphorylase. Simultaneously, glycogen synthesis is activated. 

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