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 did treating cells with DPN or with BTA alter the response to glucose concentration?
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Biology: The Unity and Diversity of Life
- Bodybuilders use a variety of anabolic substances to gain mass. Two such compounds are insulin and trenbolone. Insulin has significant anabolic and anti-catabolic properties and impacts the metabolism of various macromolecules, not just that of carbohydrates. Trenbolone binds the androgen receptor with an affinity five times higher than that of testosterone and is popular for its fat-burning and anabolic properties. H. Trenbolone C18H2202 Insulin C257H383NosO77S6 How do the different targets, mechanisms of action and durations of each drug ultimately lead to the same desired effect (increase in lean body mass)?arrow_forwardIn 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_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_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_forwardNovolog differs from "normal" insulin in that: Select one: a. An aspartic acid has been substituted for proline at B28 b. The proline at B28 and the lysine at B29 have been reversed c. A glycine has been substituten in at A21, and two new arginines have been added as B31 and B32 d. A "C-peptide" chain has been added e. The usual insulin molecule has been combined with zinc isophanearrow_forward
- Human Physiology: From Cells to Systems (MindTap ...BiologyISBN:9781285866932Author:Lauralee SherwoodPublisher:Cengage Learning