A researcher wanted to create a loss of function mutation for studying Type I Diabetes in a model animal. What mutation would mimic Type I diabetes? Down regulation of GLUT4 transporters in muscles Up regulation of insulin receptors on the pancreas O Inhibition of sugar absorption in the small intestine O Inhibition of pancreatic beta-cells

A researcher wanted to create a loss of function mutation for studying Type I Diabetes in a model animal. What mutation would mimic Type I diabetes? Down regulation of GLUT4 transporters in muscles Up regulation of insulin receptors on the pancreas O Inhibition of sugar absorption in the small intestine O Inhibition of pancreatic beta-cells

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter5: The Inheritance Of Complex Traits

Section: Chapter Questions

Problem 19QP: Researchers set up an obesity study in which MZ and DZ twins who served in the armed forces were...

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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?
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.
Regulation in biological systems depends on feedback .which is an exmple of in formation flow. when diabbetes destroy insulin-producing cells, what infortamtion flow in disrupted? The body is unable to send signals that indicate the amount of sugar in the blood. Cells in the bladder are no longer able to send signals when the blodder fills. Appetite signals no longer regulate feeding . The pancres is unable to produce enzymes to break down protein.
Obesity research has shown that about one in 1,000 people has a genetic disorder called leptin resistance. This occurs due to a mutation in the gene that codes for:
Choose the correct. Insulin inhibits this catabolic process:A. Conversion of protein to aminoacidsB. Conversion of aminoacids to proteinsC. Conversion of glucose to fatty acidsD. GlycogenesisE. Conversion of fatty acids to triglycerides
Many diabetics do not respond to insulin because of a deficiency of insulin receptors on their cells. How does this aff ect (a) the levels of circulating glucose immediately after a meal and (b) the rate of glycogen synthesis in muscle?
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
How would a mutation in G-alpha that increases its GTPase activity affect liver cell responses to epinephrine? It would decrease glucose production. It would decrease proliferation. It would increase proliferation. It would increase glucose production.
Susan has type 1 diabetes. One day, after accidentally injecting herself with too much insulin, she started to shake and feels confused. Following her doctor's suggestion, she drinks a glass of orange juice (a ready source of glucose). Soon her symptoms subside. What caused her symptoms? How would a glucose-rich snack help?
Insulin and glucagon are controlled by negative feedback mechanisms. Put them in the right order from when you eat. a)Glucose enters the bloodstream faster than the cell can use it. b) Glucose levels rise. c) Beta cells of pancreas are stimulated to release insulin into blood. d) Cells take up glucose. e) Cells of the liver convert glucose to glycogen f) The level of glucose in blood stream returns to normal.
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?
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?