NUTR 600 Exam 1

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  1. Describe the basic sequence of a generic signaling cascade: 4 steps and 4 outcomes
    1. Hormone binds to EC part of receptor activating2. Transducer (ex. G protein) which either directly activates protein kinase or activates3. Effector enzyme which then activates protein kinase4. Protein kinase phosphorylates hydroxyl group of target protein, leading to:Change in:1. Enzyme activity2. Protein-protein interactions3. Transporter activity4. Gene expression
  2. Name the types of regulation (5)- first three, from fastest to slowest and name timepoints.- last two - give examples
    1. Allosteric - immediate (effector changes shape of substrate binding site)2. Covalent modification (i.e. (de)phosphorylation) of proteins catalyzed by protein kinases & phosphatases. seconds to minutes. Phosphate's negative charge alters enzyme shape/conformation. 3. Gene expression - hours to days.4. Permanent compartmentation (DNA transcription is only in nucleus)5. Variable compartmentation (GLUT 4)
  3. Which amino acids can be phosphorylated? By which enzymes?
    1. Threonine, serine, and tyrosines of certain proteins. 2. PKA, PKC, and calmodulin activated kinase.
  4. What type of receptor is the insulin receptor? The glucagon receptor?
    Insulin receptor - single spanning receptor w/ tyrosine kinase activity.Glucagon receptor - 7-transmembrane G-protein coupled receptor
  5. What protein activates recruitment of GLUT 4 transporters from IC pool to cell membrane? What facilitates activation of original protein?
    PIP3. (1) Insulin binds to EC domain of single spanning receptor(2) Insulin binding causes change in conformation of receptor(3) This leads to autophosphorylation of tyrosines on IC domain (B-subunit) of receptor(4) Tyr-P phosphorylate tyrosines on IRS (Insulin Receptor Substrates) esp 1 &2.(5) IRS activates PIK3 which phosphorylates PIP2 to PIP3.(6) PIP3 goes on to either activate Akt or recruit glucose transporters (GLUT 4) to membrane .
  6. T or F: Is dimerization necessary for the insulin receptor to work?
  7. What types of effects does insulin have?  How long?
    Has covalent modifications (in the form of phosphorylation) which take sec to min.Also affects gene transcription, which can take hours to days.
  8. How are actions of insulin terminated?
    By dephosphorylation of receptor
  9. Name tissues that have insulin-independent systems:
    cardiac tissue, cells of nervous system, erythrocytes, cornea, muscle, hepatocytes, renal tubules, intestinal mucosa, etc. 
  10. On what amino acids can phosphorylation occur? Via which 3 enzymes?
    • 1. Tyrosine residues on certain proteins
    • 2. Serine
    • 3. Threonine

    Via PKA, PKC, calmodulin-activated kinase.
  11. Describe the signaling pathway for insulin:
    • 1. Insulin binds to a-subunit (EC domain) of insulin receptor
    • 2. Binding causes conformational change on B-subunit (tyrosine kinases) which auto-phosphorylate the 2nd B-subunit, activating the insulin receptor.
    • 3. Activated insulin receptor p'lates IRS-1 & IRS-2 (insulin receptor substrate) forming scaffold for other proteins to bind to
    • 4. This activates PI3 Kinase: PIP2--> PIP3, activating Akt
    • 5. Active Akt activates PP1, glycogen/protein synthesis, and activates transcription factors for cell proliferation, mitogenesis, gene transcription (increases/decreases). 
  12. What are actions of glucagon on macronutrients? Main goals and specific actions!
    • ·        
    • Goals:

    • o   
    • Carbs: Increase glucose concentration via
    • glycogenolysis in liver & gluconeogenesis

    • o   
    • Lipids: Increase energy availability & use
    • via TAG hydrolysis, FA oxidation, ketone body formation.

    • o   
    • Proteins: Increase AA availability to liver for
    • GNG via muscle protein hydrolysis & aa uptake by liver.

    • ·        
    • Insulin can turn off the glucagon signal by
    • activating a phosphodiesterase converting
    • cAMP à AMP (inactive). ·        
    • Goals:

    • Carbs: Increase glucose concentration via
    • glycogenolysis in liver & gluconeogenesis

    • Lipids: Increase energy availability & use
    • via TAG hydrolysis, FA oxidation, ketone body formation.

    • Proteins: Increase AA availability to liver for
    • GNG via muscle protein hydrolysis & aa uptake by liver.
  13. If someone has insulin resistance and they're given insulin in an IV, do they need more or less IV glucose to maintain normal blood glucose concentration? Why?
    • 1. Less
    • 2. B/c insulin will not be able to decrease glucose levels as effectively. 
  14. Explain how G-coupled protein receptors work with glucagon
    • 1. Peptide hormone interacts with receptor, releasing G protein
    • 2. G protein activates adenylate cyclase
    • 3. Active adenylate cyclase converts ATP--> cAMP
    • 4. cAMP activates PKA which phosphorylates its target proteins. 
  15. How does insulin affect the glucagon signal?
    It can turn off the glucagon signal by activating a phosphodiesterase that converts cAMP into AMP (inactive form). 
  16. What is an example of another hormone that works by 7-transmembrane G-coupled protein receptor?

    Explain its signaling pathway. 6 steps!

    • 1. Acetylcholine binds to 7-transmembrane receptor, changing conformation, releasing G protein
    • 2. G protein activates phospholipase C
    • 3. PLC hydrolyzes PIP2 in plasma membrane to DAG + IP3.
    • 4. IP3 causes Ca2+ release
    • 5. Ca2+ + DAG --> activation of PKC which goes on to p'late other target proteins.
    • 6. Ca2+ can also activate calmodulin-dependent kinase
  17. What symptoms are seen in nondiabetics w/ insulin resistance?
    Hyperinsulinemia & normal glucose concentration

    More insulin is required to maintain normal serum [glucose]
  18. What is the definition of insulin resistance?
    physiological condition in which more insulin than normal is required to get glucose into cells.
  19. What causes insulin resistance? Name 5 examples

    **specifically name one seen in obesity. 
    Any defect in hormone-receptor signaling pathway

    • 1. Altered hormone that binds poorly to insulin receptor
    • 2. Defective receptors
    • 3. Decreased # of receptors
    • 4. Abnormal IC signaling molecules (PI3-K, Akt)
    • 5. Abnormal phosphotylation that prevents activation of target proteins (this happens in obesity!!!)
  20. Where are GLUT 4 transporters found?
    adipocytes, skeletal myocytes, cardiac myocytes
  21. Difference b/t receptors and transporters?
    Receptors: need to interact w/ downstream event & bind to signaling molecules & do not allow passage of molecule into cell & specific w/ very high affinity for one molecule. 

    (but, may bind to others w/ lower affinities)

    Transporters : Not always specific --> can have same affinity for different molecules & allows molecules to pass through
Card Set:
NUTR 600 Exam 1
2012-09-23 04:22:34
nutr 600 exam hormones biochemistry

exam 1
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