Concept explainers
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
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?
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Chapter 34 Solutions
Biology: The Unity and Diversity of Life (MindTap Course List)
- 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?arrow_forwardOverexpression of this receptor in the cells of the adrenal gland causes Cushing's syndrome, a disease caused by the overproduction of cortisol. One strategy that scientists have employed to treat this disease is the use of small molecules that bind to, but do not activate, MC2R. This type of molecule is generically referred to as an antagonist. How can an antagonist bind to the same receptor as ACTH but not activate it? O a. The antagonist can bind covalently while ACTH binds non-covalently O b. The antagonist is only partially complimentary to the binding pocket of MC2R O The antagonist binds to ACTH and blocks it from binding to the receptor properly O d. The antagonist is the exact same structure as ACTH but since it is synthetic it doesn't work One cause of Cushing's syndrome is the inappropriate production of GPCRS in the adrenal gland that are not normally present in those cells. When these receptors are activated they result in the production of cortisol. Which statement about…arrow_forwardBased 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 inactivatedarrow_forward
- 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.arrow_forwardOne such laboratory study investigated the binding of a hormone to three different receptor proteins in the cell membrane. The data collected are shown in the table below 1) Provide a brief explanation as to why ligand binding toproteins must be a reversible process. 2) Calculate the dissociation constant (Kd) for the hormone binding to each of the three proteins.arrow_forwardThyroid hormone is produced within spherical shape structures in the thyroid gland known as 3. 1_ _ _This structure consists of an outer layer of 3.2 epithelial cells and an inner section known-as 3.3___ . This inner section is filled with 3.4 ____ that is synthesised and secreted by-the cells and contains many tyrosine residues. Within this inner section, organification occurs when 3. 5 ____ molecules attach to these tyrosine residues forming either 3. 6____ (with one molecule attacl1ed) or 3. 7____(with two molecules attached). Through coupling, T3 and T4 are also formed. Of these two hormones;- 3. 8 ____is less potent but forms approximately 93% of the metabolically active hormones secreted the thyroid gland.arrow_forward
- Human growth hormone binds to a cell-surface membrane protein that is not a receptor tyrosine kinase. The intracellular domain of the receptor can bind other proteins inside the cell. Furthermore, studies indicate that the receptor is monomeric in the absence of hormone but dimerizes on hormone binding. Propose a possible mechanism for growth-hormone signaling.arrow_forwardSuppose that you had a monoclonal antibody that recognized phosphotyros- ine. How would you expect that antibody to affect insulin signaling?arrow_forwardIn muscle cells, when adrenaline binds to beta-adrenergic receptor, it trigger signaling cascade leading to active glycogen phosphorylate breaks up glycogen into glucose subunits (Glycogen -> G1P). Base on following figure, describe this signaling cascade:arrow_forward
- Assume you have a monoclonal antibody specific for phosphotyrosine. How do you anticipate the antibody affecting insulin signalling?arrow_forwardThe physiological effects of epinephrine should in principle be mimicked by addition of cAMP to the target cells. In practice, addition of cAMP to intact target cells elicits only a minimal physiological response. Why? When the structurally related derivative dibutyryl cAMP (shown below) is added to intact cells, the expected physiological response is readily apparent. Explain the basis for the difference in cellular response to these two substances. Dibutyryl cAMP is widely used in studies of cAMP function.arrow_forwardName 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.arrow_forward
- Human Physiology: From Cells to Systems (MindTap ...BiologyISBN:9781285866932Author:Lauralee SherwoodPublisher:Cengage Learning