In the liver, insulin signalling up-regulates glycolysis. Which of the following signalling pathways explains that mechanism?Group of answer choicesIt activates protein phosphatase-1 which dephosphorylates glycogen phosphorylase.It results in the activation of cAMP dependent protein kinase A (PKA) which phosphorylates pyruvate kinase.It activates the expression of hexokinase, PFK-1 and pyruvate kinase.It results in an increased expression of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase.

Insulin signalling results in which of the following? Autophosphorylation of the G protein-coupled receptor which triggers a signalling cascade that stimulates the movement of GLUT4 towards the plasma membrane. Insulin signalling does not involve G proteins A decrease in the amount of fructose-6-phosphate converted to fructose-1,6-bisphosphate by L-phosphofructokinase-1. It activates a protein phosphatase which dephosphorylates glycogen phosphorylase to enhances the release of glucose from glycogen.

In the liver, adrenaline signalling results inGroup of answer choicesDephosphorylation of glycogen synthase which decreases glycogenesis.The T state of Phosphofructokinase-1 is stabilised which increases glycolysis.Phosphorylation of the bifunctional PFK-2/FBPase-2 enzyme which increases glycolysis.Phosphorylation of glycogen phosphorylase which increases glycogenolysis.

When insulin is released it causesGroup of answer choicesThe liver to decrease fatty acid synthesisMuscle and adipose tissue to increase glucose uptakeThe liver to decrease glucose uptakeLiver and muscle to increase glycogen breakdown

n muscle tissue, adrenaline signalling results inGroup of answer choicesDephosphorylation of the bifunctional PFK-2/FBPase-2 enzyme which increases glycolysis.Phosphorylation of glycogen phosphorylase which decreases glycogenolysis.Increased levels of fructose-1,6-bisphosphate production, which allosterically upregulates pyruvate kinase.The R state of phosphofructokinase-1 is not stabilised which decreases glycolysis.

Glycolysis and gluconeogenesis are tightly regulated, opposing metabolic pathways that help control blood glucose levels.  Glycolysis converts glucose to two pyruvate molecules, whereas gluconeogenesis consumes a net total of 6 NTPs (4 ATPs and 2 GTPs) to convert two pyruvate molecules back to glucose.  When glycolysis is upregulated, gluconeogenesis is downregulated, and vice versa.As shown in Figure 1, glycolysis and gluconeogenesis in the liver are largely regulated by the allosteric action of the small molecule fructose-2,6-bisphosphate (F2,6BP) on the enzymes phosphofructokinase-1 (PFK-1) and fructose-1,6-bisphosphatase (F1,6BPase).  PFK-1 is a kinase that uses ATP to phosphorylate fructose-6-phosphate (F6P) in an irreversible step of glycolysis, forming fructose-1,6-bisphosphate (F1,6BP) and ADP.  During gluconeogenesis, F1,6BPase removes the phosphate group by hydrolysis.Figure 1  Activities of (A) PFK-1 and (B) F1,6BPase on their respective substrates in the presence (solid lines) and absence (dashed lines) of F2,6BPA bifunctional enzyme that contains a phosphofructokinase-2 (PFK-2) domain and a fructose-2,6-bisphosphatase (F2,6BPase) domain controls F2,6BP levels in the liver.  The PFK-2 domain converts F6P to F2,6BP, and the F2,6BPase domain converts F2,6BP back to F6P.  When blood glucose levels are low, the enzyme becomes phosphorylated.  This phosphorylation event simultaneously activates the F2,6BPase domain and inactivates the PFK-2 domain.  Under high blood glucose conditions, the enzyme becomes dephosphorylated, activating the PFK-2 domain and inactivating the F2,6BPase domain.Question 13Which metabolic process most likely provides the energy necessary for sustained gluconeogenesis?A.Fatty acid oxidationB.GlycogenolysisC.FermentationD.Pentose phosphate pathway