Biochemistry
9th Edition
ISBN: 9781319114671
Author: Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher: W. H. Freeman
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Which of the following is a consequence of insulin signaling?
(select all that apply)
Cell growth/division genes upregulated |
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Increased cellular glucose uptake through GLUT4 transporter |
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glycogen degradation |
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Glucose synthesis |
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- Which of these enzymes/complexes will insulin activate in the liver? Choose all that apply. Glycogen synthase Glycogen phosphorylase Acetyl-CoA carboxylase Carnitine shuttle PFK-1 FBPase-1arrow_forwardHow can we make an implantable, glucose-sensitive microvalve to control insulin delivery for diabetic patients?arrow_forward1. Please explain the picture using the following terms: Receptor, (G protein or ligand-gated ion channel) Protein kinases and phosphorylation Secondary messengers Response (DNA to protein = expression of a protein/trait/action by a cell)arrow_forward
- Which of the following are the effects of insulin on skeletal muscle cells and which are not? Which are the effects of insulin on adipocytes? Inhibits gluconeogenesis Inhibits lipolysis Stimulates glucose entry into cell Stimulates glycogenolysis Stimulates triglyceride synthesisarrow_forwardThis is a question assigned after reading the case study available here https://sciencecases.lib.buffalo.edu/files/statins.pdf HMG CoA reductase is activated by insulin signaling, and inhibited by glucagon signaling. Explain why insulin resistance and type II diabetes often are accompanied by elevated cholesterol levels.arrow_forwardWhat protein is activated in the cytoplasm due to activation of the insulin receptor? protein kinase A glycogen phosphorylase protein phosphatase 1 glycogen synthase kinase insulin-receptor substratearrow_forward
- Humans may have Rh+ blood or Rh- blood. A person who is Rh+ (R) has a certain type of protein on the red blood cells. A person who is Rh- (r) does not have this particular protein. In humans, Rh+ dominates Rh-. Normal insulin (I) production dominates abnormal insulin production (i) (diabetes). If both parents are heterozygous for both Rh+ and normal insulin production, what phenotypes would they produce in their offspring? What are the probabilities of producing each phenotype?arrow_forwardWhich of the following are mechanisms that prevent the liver from using up glucose that is more urgently required by other tissues? (select all that apply) Group of answer choices Glucokinase (the liver's version of hexokinase) has a lower affinity for glucose than hexokinase does GLUT2 has a lower affinity for glucose than GLUT4 does The liver produces insulin when blood glucose levels are low The liver does not express a phosphofructokinase enzyme The liver increases glycolysis in response to glucagonarrow_forwardWhich processes are involved in the signaling pathway from insulin to glycogen synthase kinase 3 (GSK3) inactivation (select all that apply)? O protein kinase B being activated by a protein kinase known as PDK-1 O activation of insulin receptor substrate-1 (IRS-1) by phosphorylation O phosphatidylinositol 3-kinase associating with IRS-1 generates phosphatidylinositol 4,5-bisphosphate O protein kinase B phosphorylating GSK3, resulting in its activation O insulin binding to a tyrosine kinase receptorarrow_forward
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