How does insulin cause an increase in the rate of glucose transport into cells when blood glucose levels are elevated? causes recruitment of glucose transporters from intracellular vesicles to the cell membrane causes activation of Na/K ATPase to increase glucose active transport binds to the glucose transporter on the cell membrane causing a conformational change resulting in greater transport velocity activates an insulin-dependent porin that allows for rapid glucose transport

How does insulin cause an increase in the rate of glucose transport into cells when blood glucose levels are elevated? causes recruitment of glucose transporters from intracellular vesicles to the cell membrane causes activation of Na/K ATPase to increase glucose active transport binds to the glucose transporter on the cell membrane causing a conformational change resulting in greater transport velocity activates an insulin-dependent porin that allows for rapid glucose transport

Biology: The Unity and Diversity of Life (MindTap Course List)

15th Edition

ISBN:9781337408332

Author:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Publisher:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Chapter34: Endocrine Control

Section: Chapter Questions

Problem 2DAA: Effect of BPA on Insulin Secretion Bisphenol A (BPA) is an endocrine disruptor that may increase the...

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Effect of BPA on Insulin Secretion Bisphenol A (BPA) is an endocrine disruptor that may increase the risk of type 2 diabetes. Angel Nadal suspected that BPA disrupts insulin metabolism by activating an estrogen receptor on pancreatic islet cells. FIGURE 34.11 shows the results of one experiments. Cultured cells from human pancreatic islets were exposed either to BPA or to DPN, a chemical that binds to the estrogen receptor and activates it. Cells were then exposed to glucose, and their insulin Secretion was monitored. FIGURE 34.11 Effects of BPA and DPN on glucose-stimulated insulin secretion. DPN is a chemical known to bind and activate estrogen receptors on pancreatic cells. A glucose concentration of 8 millimolar (mM) is equivalent to that of the blood after a meal. Is this data consistent with the hypothesis that BPA alters human insulin secretion by binding to and activating the estrogen receptor?
Effect of BPA on Insulin Secretion Bisphenol A (BPA) is an endocrine disruptor that may increase the risk of type 2 diabetes. Angel Nadal suspected that BPA disrupts insulin metabolism by activating an estrogen receptor on pancreatic islet cells. FIGURE 34.11 shows the results of one experiments. Cultured cells from human pancreatic islets were exposed either to BPA or to DPN, a chemical that binds to the estrogen receptor and activates it. Cells were then exposed to glucose, and their insulin Secretion was monitored. FIGURE 34.11 Effects of BPA and DPN on glucose-stimulated insulin secretion. DPN is a chemical known to bind and activate estrogen receptors on pancreatic cells. A glucose concentration of 8 millimolar (mM) is equivalent to that of the blood after a meal. How were the effects or DPN and BPA similar? How did they differ?
The hormone insulin enhances the carrier-mediated transport of glucose into most of the bodys cells but not into brain cells. The uptake of glucose from the blood by neurons does not depend on insulin. Knowing the brains need for a continuous supply of blood-borne glucose, predict the effect that insulin excess would have on the brain.
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
Which of the following is the primary process by which insulin stimulates glucose transport into adipose tissue cells?A) Activating Na+-K+ ATPaseB) Increasing synthesis of the glucose transporterC) Phosphorylating glucose to maintain the gradient of free glucose across the cellD) Promoting movement of the glucose transporter from the cytoplasm to the cell membrane
By what mechanisms are GLUT transporters added to the membrane of insulin-dependent cells after insulin binds to its receptor? -endocytosis -exocytosis -facilitated diffusion -paracellular transport -transcytosis Don't copy from Google i need unique answer
Chronic 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.
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 B
People with non-insulin-dependent diabetes mellitus are generally not ketosis prone. This is thought to be a result of: the lack of increase in glucagons in the se individuals the presence of insulin in the individuals their obesity the fact that, their blood glucose levels do not tend to rise significantly Metabolic actions of insulin include all of the following except: increased glycogenesis decreased gluconeogenesis increased basal metabolic rate increased skeletal muscle amino acid up-take all of the above are metabolic actions of insulin
Insulin binding to its cellular receptor causes dimerization and phosphorylation of ( ) and assembly of a ( ) membrane transporter.
Which of the following enzymes are activated after insulin binds to its receptor? (select all that apply) Protein Phosphatase-1 Glycogen Synthase Lipase Acetyl CoA Carboxylase Glycogen phosphorylase Glycogen phosphorylase kinase
All of the following molecules are involved in insulin signal transduction except a. IRS b. RAS c. ANF d. PIP3