Glucose from glycogen

No ATP is required to remove glucose from glycogen stores. Degradation 1... 

Although the idea of the steric fit of substrate to enzyme was a powerful one, in detail it presented some problems. One of these, the notion that the enzyme should fit the transition state better than it fits the substrate, has already been mentioned. The most severe of the problems, however, was illustrated with the chemistry of phosphorylase. Why was the enzyme specific for the transfer of glucose from glycogen Why did it not catalyze the... 

Salicylic acid, the major metabolite of aspirin, uncouples the electron transport chain in the mitochondria. This results in (a) increased use of oxygen and production of carbon dioxide, (b) lack of ATP, and (c) excess energy no longer utilized in ATP production. The result is increased respiration and raised temperature. The alterations in respiration lead to alkalosis followed by acidosis. The lack of ATP and loss of respiratory control will cause increased metabolic activity and hypoglycemia after an initial mobilization of glucose from glycogen. 

Epinephrine prepares the body for increased activity by mobilizing blood glucose from glycogen and other precursors. 

Adenylate cyclase, which converts ATP to adenosine 3, 5 -cyclic monophosphate (cAMP) is activated by receptors that activate the G-protein known as Gs (for stimulatory G-protein) and inhibited by receptors that activate the G-protein known as G, (for inhibitory G-protein). Elevation of cAMP levels underlie the release of glucose from glycogen that is induced by epinephrine and glucagon (see Chap. 11). 

Glycogen is not as reduced as fatty acids are and consequently not as energy rich. Why isn t all excess fuel stored as fatty acids rather than as glycogen The controlled release of glucose from glycogen maintains blood-glucose levels between meals. The circulating blood keeps the brain supplied... 

The first step in the liberation of glucose from glycogen is phosphorolysis of a glucosyl residue at one of the terminal, nonreducing ends of the glycogen macro-... 

The first cAMP-mediated cellular response to be discovered—the release of glucose from glycogen—occurs in muscle and liver cells stimulated by epinephrine or other... 

In liver and muscle cells, epinephrine stimulates the release of glucose from glycogen by Inhibiting glycogen synthesis and stimulating glycogen breakdown. Outline the molecular events that occur after epinephrine binds to its receptor and the resultant Increase in the concentration of intracellular cAMP. How are the cAMP levels returned to normal Describe the events that occur after cAMP levels decline. 

Glucagon and the liver. The action of glucagon on the liver is shown above. The major overall effect is an increase in blood glucose, from glycogen and gluconeogenesis, and an increase in ketone bodies (see text for more detail). Major allosteric and covalent effects are shown, with the final form of covalently converted enzymes shown in purple, and reactions increased by glucagon shown with purple arrows and those slowed shown with dashed lines (see text for... 

Fig 8. Production of blood glucose from glycogen (by glycogenolysis) and from alanine, lactate, and glycerol (by gluconeogenesis). PEP = phosphoenolpyruvate OAA = oxaloacetate. 

Am. The hormones epinephrine and glucagon cannot penetrate cell membranes. They affect metabolic processes by binding to specific receptors on the membrane, which receptors in turn activate a specific enzyme bound to the inner membrane surface, adenylate cyclase. This enzyme converts ATP to cyclic AMP (cyclic adenosine monophosphate), or c-AMP. The presence of c-AMP activates another enzyme, protein kinase, which phosphorylates and activates phosphorylase kinase. Phosphorylase kinase phosphorylates phosphorylase b (inactive) to form phosphorylase a (active) which in turn cleaves glucose from glycogen by phosphorolysis to yield glucose-I-PO4. 

---