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- Describe all the sources of amplification in the insulin receptor system.Identify the partial sequence of events that occurs after the insulin binds to its receptor. 1. Phosphorylation of insulin receptor substrate (IRS-1) 2. Activation of the receptor tyrosine kinase activity 3. Activation of phosphodiesterase 4. Activation of phospholipase C 5. Phosphorylation of phosphatidylinositol 6. Activation of phosphatidylinositol-3 -kinase (P1-3 kinase) 7. Binding of Grb 2 8. Activation of a phosphatase 9. Dephosphorylation of pyruvate kinase 10. phosphorylation of pyruvate kinase 2-7-1-4-3-9 1-7-3-5-6-8 2-1-6-5-8-9 2-7-1-6-5-8-9 2-7-4-6-1-8-10Describe the cascade, in detail, what follows hormone activation in the PIP2 cascade. Be sure to describe in detail the G Protein action, and the three second messengers in this system.
- Explain the hormone induced signal transduction events leading to regulation of Phosphofructokinase II (PFKII) during the fed, fasted and stress states.People with non-insulin-dependent diabetes mellitus are generally not ketosis prone. This is thought to be a result of: the lack of increase in glucagons in the se individuals the presence of insulin in the individuals their obesity the fact that, their blood glucose levels do not tend to rise significantly Metabolic actions of insulin include all of the following except: increased glycogenesis decreased gluconeogenesis increased basal metabolic rate increased skeletal muscle amino acid up-take all of the above are metabolic actions of insulinThis 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.
- Discuss the synthesis and breakdown of glycogen and how the processes are regulated in response xto hormone action. also describe the various types of glycogen storage diseasesIn Diabetic patients, the excess glucose is converted into O-linked-N- Acetylglucosamine. This byproduct causes vascular complications by reducing the release of from vessel endothelial cells. O insulin O nitric oxide O epinephrine O carbon dioxideDescribe the mechanism of action of insulin. Based on the MOA, when would insulin be contraindicated?
- For both T1DM and T2DM, describe the following: Causes Symptoms Treatments Glucose levels Insulin levels Insulin receptor sensitivity Also please discuss the cause/effect relationship between acute and chronic stress (chronic disease or homelessness, for instance) and T1DM and T2DM. What is the mechanism by which the nervous system impacts stress hormones? Are there neurotransmitters involved? Which neurotransmitters? Which stress hormones?Explain the structure and location of the cellular receptor and describe in detail the mechanism of action of steroid hormones. Compare this to the structure and function of the insulin receptor. What properties are different between the ligands? What cellular responses occur to each as a result of receptor activation. Describe the pathways and relate to specific examples. please explain me in detail.Describe one insulin-mediated mechanism that normally increases glucose uptake into skeletal muscle and adipose tissue when blood glucose levels are high (but would not be operational in T1DM patients)
