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8 Cards in this Set

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Explain how the fasting state promotes gluconeogenesis.

Blood glucose is low, brain needs glucose, so liver releases glucose into the bloodstream. High glucagon/insulin ratio causes elevated cAMP and increased levels of active protein kinase A. Increase PKA activity favors the phosphorylated form of the PFK2/ FBP 2 complex. Phosphorylated PFK 2 is inactive, whereas FBP is active. This impedes the formation of F2,6-B.

Increased glucagon activates PKA, which phosphorylates the liver form of pyruvate kinase & inactivates it; inactivating glycolysis!

Explain control mechanisms that ensure that glycolysis does not occur simultaneously with gluconeogenesis.

Regulatory steps unique to each pathway that drive rxns forward for either glycolysis or gluconeogenesis. Ex: either hexokinase or glucose 6-phosphatase active, either PFK 1 or fructose 1,6-bisphosphatase-1 active, either pyruvate kinase or pyruvate carboxylase active.

The levels of ATP/AMP, insulin/glucagon and certain intermediates activate/inhibit glycolysis or gluconeogenesis. (Ex: high ATP, citrate, Acetyl CoA, fatty acids, and glucagon inhibits glycolysis and activates gluconeogenesis).

Explain why gluconeogenesis requires energy input, compared to glycolysis which yields energy.

ATP is needed to drive certain reactions of gluconeogenesis. Gluconeogenesis is highly endergonic until coupled to the hydrolysis of ATP or GTP, effectively making the process exergonic.

Explain how alcohol intoxication can cause hypoglycemia.

Ethanol is oxidized, via the action of alcohol dehydrogenase and aldehyde dehydrogenase to acetate. Acetate is poorly utilized metabolically.

Excess NADH generated can lead to the chemical reduction of pyruvate and oxaloacetate, limiting their availability as substrates for gluconeogenesis.

Describe features of glycogen that allow its glucose (Glc) residues to be rapidly and efficiently mobilized.

Primary linkage is 1,4 and branches spaced 8-10 sugars. Anchored 1,6 linkages. Can have 12 branches. Glc molecules are stored as branched, water soluble polymer. Avoids osmotic consequences of storing them as individual molecules yet ensures accessibility. Each glycogen molecule exists as discrete cytoplasmic granule of up to 400,000 monosaccharide units and associated metabolic processing enzymes.

Phosphorolysis of glycogen cleaves the a 1,4 bond, pulling off phosphorylated glucose ready to use for glycolysis! Debranching enzyme cleaves a 1,6 bond, producing free glucose.

Explain how the fasting state (low blood glucose) promotes glucose release from the liver by glycogenolysis.

Low blood glucose --> low insulin, high glucagon --> glucagon activates adenylate cyclase --> activates cAMP --> activates pyruvate kinase A --> activates glycogen phosphorylase kinase A --> activates glycogen phosphorylase A to degrade glycogen & release glucose.

Glucagon also activates FBPase-2, which inactivates PFK2, decreasing the amount of F26BP (because PFK2 makes F26BP), inhibits glycolysis and stimulates gluconeogenesis.

Explain how glycogenesis and glycogenolysis are inversely and oppositely regulated by insulin and glucagon.

High blood Glc: Insulin inactivates glycogen synthase kinase 3 (GSK3) by phosphorylation so that glycogen synthase is not inactivated & allows glucose to be stored in the cells (glycogenesis).

Low blood Glc: absence of insulin, active GSK3, phosphorylates glycogen synthase and inactivates it. Utilization of glucose for immediate need, not storing it. Glucagon/Epi keep glycogen synthase inactive. Glucagon and Epi converts glycogen phosphorylase to active form by phosphorylation through phosphorylase b kinase. Now glycogen phosphorylase can pull of glucose from glycogen to use!

Explain how glycogenolysis and glycolysis are coordinately regulated in muscle.

Insulin brings glucose into the muscle cell. Insulin activates hexokinase (glycolysis). Insulin also activates glycogen synthase. This inactivates glycogenolysis. See above for more explanation.

Epinephrine ultimately causes the break down of glycogen (glycogenolysis) so that glucose 1-phosphate can be used for glycolysis in order to produce a muscle contraction.