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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How does the Na+/ K+ ATPase play a role in glucose transport? phosphorylates GLUT1 to activate it pumps Na+ across plasma membranes into cytoplasm to activate the sodium-glucose transporter pumps Na+ across basal plasma membrane to the outside of intestinal cells so that co-transport of glucose with Na+ into cytoplasm is facilitated allows for the diffusion of K+ inside of cell so that co-transport with glucose is facilitated
If our body lack of insulin, is it mean the glucose in our blood is low concentration now. So is it will effect pathways in mucles cell like glycolysis, fatty acids synthesis, glycogen synthesis, gluconeogenesis (increase or decrease)? I know the liver can regconize that low or high concentration of blood glucose so insulin or glucagon can act as the signal for liver can know, but is the muscle cell can do it to? If not, how they know to adjust their pathways. And if our body lack of insulin, is the liver cells response same as glucagon signaling.
Which of the following is NOT regulated by glucagon? Glut-4 transporters O protein kinase A O Phosphorylase O Hormone sensitive lipase O Gluconeogenesis
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
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
Given insulin's structure, where is its target likely located? Insulin's adverse side effects include headache, nau- sea, hunger, confusion and weakness. What can these symptoms be attributed to? Insulin has major effects on muscle and adipose tissue. It increases the rate of glucose transport across the cell membrane, decreases the rate of lipolysis, and increases uptake of triglycerides and some amino acids from the blood. In doing so, what metabolic processes does it favor? Carbohydrates: Lipids: Proteins:
GluT transporters are responsible for passive transport of Glucose into the cell to yield G-6-P that cannot exit the cell; in liver cells this process is always regulated by insulin. True or False
what type of glucose transport protein is found in pancreatic beta cells? SGLUT-1 GLUT-2 GLUT-3 GLUT-4 GLUT-5
Digoxin, 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 O Failure to transport glucose into cells after after eating a large meal O Enhanced response of muscle cells to Acetylcholine O Failure to transport Cl" out of the cell using direct active transport
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 did treating cells with DPN or with BTA alter the response to glucose concentration?
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?