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Based on your understanding of the binding of insulin, select all of the following events that you would expect to occur in muscle cells due to insulin binding to receptors.
Group of answer choices
a. Glycogen synthesis is activated
b. PFK is stabilized in the R-state and glycolysis is activated
c. GLUT4 (transporters) are increased in concentration at the plasma membrane
d. Fructose 2,6-bisphosphate increased levels aid in stabilization of the T-state fructose 1,6-bisphosphatase
e. Gluconeogenesis is activated in response to elevated fructose 2,6-bisphosphate levels
f. Phosphorylation cascades allow for covalent modifications that would aid in the breakdown of glycogen to allow for increased levels of glucose 6-phosphate in the cell
g. Hexokinase is inhibited so glucose will not be brought into the cell in high amounts
h. Glycogen breakdown pathway is inactivated
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- Insulin signals activate all of the following enzymes except: Phosphoinositide 3-kinase (PI3K) Glycogen synthase kinase 3 (GSK3) Protein kinase B (PKB; or Akt) All of the above enzymes are activated by insulin signals Citrate move in and out of mitochondria via a specific transport protein. What would happen if aninhibitor completely inhibited this transport system? Fatty acid biosynthesis would slow down Ketone body synthesis would slow down Both A and B Neither A nor BWhich of the following are true about how pancreatic β cells sense blood glucose levels and release insulin? (select all that apply) Group of answer choices The first step of glycolysis (producing glucose 6-phosphate) is more efficient in pancreatic β cells than in muscle glucose transporters in pancreatic β cells have a higher affinity for glucose than the transporters in other tissues Increased production of ATP is used as a signal that blood glucose is high Insulin is released when blood glucose levels are high Increases in ATP open a K+ channel Influx of Ca2+ stimulates insulin releaseDigoxin, a toxin derived from the foxglove (shown), can be used to treat heart disorders such as atrial fibrillation. Digoxin’s mechanism of action is to inhibit the Na+/K+ ATPase. Which of the following is the most likely side effect of Digoxin treatment? Failure to transport glucose into cells during an extended fast Failure to transport glucose into cells after after eating a large meal Enhanced response of muscle cells to Acetylcholine Failure to transport Cl- out of the cell using direct active transport
- Normally, when blood glucose level increases (e.g. after a meal), the islet cells in the pancreas secrete insulin. When insulin molecules bind to insulin receptors on the surface of a muscle cell, the receptors become activated, initiating a signaling pathway which eventually results in the increase in the number of passive glucose transporter on the muscle cell surface thus increases the uptake of glucose into the cell and decrease blood glucose level. Indicate whether the following conditions/practice will likely lead to diabetes (mark Yes or No). [Select] degeneration of islet cells [Select] [Select] [Select] a mutation in the insulin receptor that increases its kinase activity ✓ exercise a mutation in the insulin receptor that prevents dimerizationGlycogenesis occurs in both muscle and liver. Select one: O True O False Glycogen is released from the muscle due to increased CAMP due to: Select one: O a. Growth hormone O b. Epinephrine O c. Thyroxine O d. Glucagon UDP-Glucose is converted to UDP-glucoronic acid by: Select one: O a. NADP O b. ATP O c. GTP O d. FAD O e. NAD In the fasted state gluconeogenesis is promote by which enzyme Select one: O a. Fructose 2,6 bisphosphate induced stimulation of phosphofructokinase-1 O b. Acteyl CoA induced stimulation of pyruvate carboxylase O c. Citrate induced stimulation of Acetyl CoA decarboxylase Glyconeogenesis prevents hypoglycemia during prolonged fasting. Select one: O True O FalseThe synthesis and degradation of glycogen in muscle is not a futile (ATP-hydrolyzing)cycle because:A. glycogen synthase and phosphorylase are simultaneously activatedB. cyclic AMP activates adenylate kinase. C. when glycogen synthase is inactivated, phosphorylase is simultaneously activated. D. glycogen binds Mg2+, thereby lowering the concentration of MgATP2-
- Compare and contrast the effects of glucagon and epinephrine on metabolic pathways in their target tissues. Keep in mind that skeletal muscle lacks cell surface receptors for glucagon.Glycogen breakdown is stimulated by a signaling cascade that is an excellent example of signal amplification. Amplification in glycogen breakdown is where a small number of signal molecules (hormones) activate a rapid and large release of glucose. Which of the following is the correct sequence for this signaling cascade in skeletal muscle cells? O epinephrine, GPCR, Protein kinase A (PKA), phosphorylase b kinase O insulin, insulin receptor (RTK), protein phosphatase-1 (PP1), glycogen phosphorylase glucagon, GPCR, Protein kinase A (PKA), glycogen synthase O epinephrine, protein phosphatase-1 (PP1), phosphorylase b kinase, glycogen synthase insulin, insulin receptor (RTK), protein phosphatase-1 (PP1), bifunctional enzyme, glycogen synthaseChronic stress or GC exposure can cause insulin resistance. The influence of GC on insulin is complex, but leads to hyperinsulinemia (high circulating insulin levels) and insulin resistance. Insulin resistance is typically caused by a decreased number of insulin receptors on the cell surface. Speculate on a mechanism resulting in a decreased number of insulin receptors.
- Which of the following are true statements about enzyme reactions occurring in a human muscle cell that has been stimulated by epinephrine? There is an amplified production of second messenger cyclic AMP. Glucagon is secreted by the muscle cell. Protein kinase A stimulates phosphorylase kinase which then stimulates phosphorylase to breakdown glycogen. GTP rather than ATP is used in the reaction that produces OAA from PEP Protein kinases remove phosphate groups from proteins. The adrenergic receptor causes the G-protein to lose GDP and bind GTPIdentify the partial sequence of events that occurs after the insulin binds to its receptor. 1. Phosphorylation of insulin receptor substrate (IRS-1) 2. Activation of the receptor tyrosine kinase activity 3. Activation of phosphodiesterase 4. Activation of phospholipase C 5. Phosphorylation of phosphatidylinositol 6. Activation of phosphatidylinositol-3 -kinase (P1-3 kinase) 7. Binding of Grb 2 8. Activation of a phosphatase 9. Dephosphorylation of pyruvate kinase 10. phosphorylation of pyruvate kinase 2-7-1-4-3-9 1-7-3-5-6-8 2-1-6-5-8-9 2-7-1-6-5-8-9 2-7-4-6-1-8-10Why is it physiologically advantageous for the pancreas to use GLUT2, with a high Ky glucose entry into ß cells? M, as the transporter that allows GLUT2 is a low-affinity glucose transporter; therefore, insulin is only released in response to elevated circulating glucose levels. GLUT2 is a low-affinity glucose transporter; therefore, glucagon is only released in response to elevated circulating glucose levels. GLUT2 is a high-affinity glucose transporter; therefore, glucagon is released continuously in response to the constant rate of glucose uptake. GLUT2 is a high-affinity glucose transporter; therefore, insulin is released continuously in response to the constant rate of glucose uptake.