Match the molecule involved in insulin signaling with what it does insulin receptor binds to insulin and sends sigı v glucose [Choose ] insulin [ Choose ] glucose transporter [ Choose ]
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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. How did treating cells with DPN or with BTA alter the response to glucose concentration?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 inactivatedInsulin binding to its cellular receptor causes dimerization and phosphorylation of ( ) and assembly of a ( ) membrane transporter.
- Describe the process that results in the activation of multiple copies of PKB in response to the binding of a single molecule of insulin to its receptor. Explain why insulin can stimulate the activation PKB of but not the activation of PK.Describe two features of insulin signaling that affect glucose utilization. Aβ-adrenergic response can be modulated through the actions of a receptorkinase and arrestin because phosphorylation by the kinase desensitizes thereceptor. How might signaling by a tyrosine receptor kinase, such as theinsulin receptor, be modulated?Pancreatic β cells express a receptor for fatty acids. Fatty acid binding to the protein appears to stimulate insulin secretion. Does this phenomenon make metabolic sense?
- In order to help Mike understand, explain how the rate of insulin release differs after consumption of simple andcomplex carbohydrates. You may choose to answer with words or a labeled diagram Now use your table to explain to Mike why elevated insulin levels are associated with heart disease.In some forms of diabetes, a mutation in the b subunit of the insulin receptor abolishes the enzymatic activity of that subunit. How does the mutation affect the cell’s response to insulin? Can additional insulin (e.g., from injections) overcome the defect?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
- Describe the process that results in the activation of multiple copies of PKBPKB in response to the binding of a single molecule of insulin to its receptor. Explain why insulin can stimulate the activation PKBPKBof but not the activation of PKPK.Receptors for _____________able to stimulate (indirectly) adenylate cyclase when bound to their respective ligand/hormone. A. glucagon B. insulin C. insulin & glucagon D. epinephrine E. epinephrine & glucagonName two proteins that are effectors of the insulin signaling pathway in adipocytes, liver, or muscle cells. Explain how these effector proteins address the conditions that triggered insulin release.