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Biochem > Week 4 > Flashcards

Week 4 Flashcards

1
Q

paracrine

A

secreted from cells not normally thought of as endocrine cells
actions performed on nearby cells

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2
Q

autocrine

A

act on cell from which it is secreted or on nearby that are the same type of cells

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3
Q

bind hydrophobic chemical messengers

A

intracellular receptors

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4
Q

usually elecit a transcriptional response

A

intracellular receptor

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5
Q

cortisol binds what type of receptor

A

intracellular

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6
Q

bind hydrophillic chemical messengers

A

membrane receptors

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7
Q

usually directly change enzyme activity through protein-protein interactions

A

membrane receptors

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8
Q

receptors that are slow to change phenotype

A

intracellular

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9
Q

receptors that are fast to change phentotype

A

membrane

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10
Q

insulin binds what type of receptor

A

membrane

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11
Q

glucagon binds what type of receptor

A

membrane

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12
Q

intracellular signals function as

A

transcription factors

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13
Q

cortisol travels through blood…

A

attached to serum albumin and steroid hormone binding globulin

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14
Q

what happens when cortisol binds to ligand

A

dimerization of the receptors
exposes nuclear translocation signal that allows hormone-receptor complex to cross the nuclear membrane into the nucleus where it acts as a transcription factor

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15
Q

cortisol is destroyed by the

A

liver

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16
Q

g-protein coupled receptor cascade uses what type of receptors

A

membrane bound

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17
Q

describe glucagon binding

A

binds to EC domain of 7-helix receptor causing conformational change that is transmitted to a G-protein on the cytosolic side. G alpha rleases GDP and binds GTP

Galph-GTP dissociate and activates adenylyl cyclase

adenylyl cyclas catalyze synthesis of cAMP which activates protein kinase A

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18
Q

what can degrade cAMP in g-protein cascade?

A

phosphodiesterase

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19
Q

Galphas causes

A

increased cAMP

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20
Q

galphai causes

A

decreased cAMP

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21
Q

galphaq causes

A

increased phospholipase C activity

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22
Q

insulin signaling

A
  • dimerize receptor tyrosine kinase receptor on ligand binding
  • active receptor phosphorylates insulin receptor substrated which binds other proteins to amplify the signal
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23
Q

what proteins does IRS bind

A

phosphoinositol kinase 1 (activated PK8)

Grb2 (activates MAPK cascade)

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24
Q

provides connection between hormone receptor and intra cellular calcium

A

phosphatidylinositide

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25
Q

phosphatidylinositide metabolism

A

Gsq activates phospholipase C which cleaves PlP2 to form inositol-1,4,5-triphosphate and diacylglycerol

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26
Q

inositol-1,4,5-triphosphate

A

enhances Ca release from ER

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27
Q

diacylglycerol

A

activate protein kinase C

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28
Q

kinases catalyze

A

sequential transfer of Pi from ATP to hydroxyl groups to yield phosphatidylinositol-4,5-biphosphate

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29
Q

insulin in fed state

A

elevated

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30
Q

glucagon in fed state

A

low

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31
Q

cortisol in fed state

A

low

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32
Q

epinephrine in fed state

A

low

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33
Q

fuel for liver in fed state

A

glucose by glut 2

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34
Q

fuel for skeletal muscle in fed state

A

glucose by glut 4

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35
Q

fuel for RBC in fed state

A

glucose by glut 1

36
Q

fuel for brain in fed state

A

glucose by glut 1 and 3

37
Q

fuel for adipose in fed state

A

glucose by glut 4

38
Q

insulin in fasted state

A

low

39
Q

glucagon in fasted state

A

elevated

40
Q

cortisol in fasted state

A

elevated

41
Q

epinephrine in fasted state

A

elevated

42
Q

fuel for liver in fasted state

A

free fa from lipolysis

43
Q

fuel for skeletal muscle in fasted state

A

free fa from lipolysis

44
Q

fuel for RBC in fasted state

A

glucose from hepatic gluconeogenesis and glycogenolysis

45
Q

fuel for brain in fasted state

A

glucose from hepatic gluconeogenesis and glycogenolysis

46
Q

fuel for adipose in fasted state

A

FA from store triacylglycerols

47
Q

insulin in liver

A 
glycolysis
TCA
glycogen synthesis
FA synthesis
protein synthesis
48
Q

insulin in skeletal muscle

A

glucose uptake thorugh GLUT 4
protein synthesis
glycogen synthesis

49
Q

insulin in adipose

A

triacylglycerol synthesis

glucose uptake through GLUT4

50
Q

glucagon in liver

A

glycogenolysis
gluconeogenesis
lipolysis
beta-oxidation of FA

51
Q

glucagon in skeletal muscle

A

no impact

52
Q

glucagon in adipose

A

lipolysis

53
Q

epi in liver

A

glycogenolysis via alpha agonist pathway
lipolysis
beta-oxidation of FA

54
Q

epi in skeletal muscle

A

glycogenolysis via cAMP pathway

55
Q

epi in adipose

A

lipolysis

56
Q

cortisol in liver

A

enhances gluconeogenesis through enhanced transcription of proteins

57
Q

cortisol in skeletal muscle

A

promotes protein catabolism to provide AA for gluconeogenesis occurring in liver

58
Q

4 hormones controlling glucose homeostasis

A

insulin
glucagon
cortisol
epinephrine

59
Q

insulin signals through

A

receptor tyrosine kinase

60
Q

glucagon signal through

A

G protein coupled receptor

61
Q

cortisol signals through

A

binding an intracellular receptor

62
Q

epinephrine signals through

A

ann additional g protein coupled receptor

63
Q

insulin will increase the activity of

A

glycolysis
glycogen synthesis
fatty acid synthesis
protein synthesis

64
Q

when insulin increases glycolysis this

A

will generate pyruvate which is used to make acetyl coa which is oxidized in the TCA

65
Q

glucagon leads to

A
  • glycogenolysis
  • gluconeogenesis
  • release of stored TAG
66
Q

supstrates for glucogenic processes come from

A

tissue proteins which are converted back into free amino acids and transaminated to carbon skeletons which are used to produce glucose

67
Q

insulin signaling

A
  • binding of ligand insulin to receptor
  • dimerization causes auto-phosphorylation event of exposed tyrosine residues which serve as docking station for insulin receptor substrate
  • other tyrosines can then be phosphorylated and serve as additional docking station for gub 2 and IP3 kinase
68
Q

docking of IP3 kinase on insulin receptor can

A

activate downstream kinase PDK1 or phosphoinositide dependent kinase

69
Q

docking of grub 2 on insulin receptor can

A

activate map kinase cascade

70
Q

primarily signal through g protein coupled receptors

A

epinephrine

glucagon

71
Q

G alpha S activated

A

adenylyl cyclase which will increase synthesis of cyclic AMP which will active protein kinase A to lead to phosphorylation
cyclic AMP is degraded to phosphodiesterase as terminating signal

72
Q

GQ subunit activate

A

phosphil APC which will cleave PIP2 into inositol triphosphate and diacylglycerol

73
Q

diacylclycerol will

A

activate protein kinase C

74
Q

IP3 will

A

enhance calcium release from the ER

75
Q 
A novel signaling cascade is discovered that you suspect activates a G-alpha s subunit.  Which of the following downstream events would be consistent with this discovery?
a)  Activation of adenylyl cyclase 
b)  Decreased synthesis of cAMP
c)  Activation of phosphodiesterase 
d)  Inhibition of adenylyl cyclase
A

A

76
Q

receptor for steroid hormones are

A

within cytosol or nucleus

77
Q

primary fuel oxidized by tissues in fed state

A

glucose

78
Q

glucose uptake in liver

A

glut2 transporter uptakes in insulin-independent manner - glut2 always present whether insulin is present or not

79
Q

glucose uptake in skeletal muscle and adipose

A

insulin-dependent by glut4

80
Q

glucose is oxidezed by

A

glycolysis

81
Q

A young woman goes to work without eating breakfast and skips lunch. In this scenario, which of the following pathways is providing substrates being used to generate ATP in the liver?

a) Free fatty acids
b) Glucose from hepatic glycogenolysis
c) Blood glucose
d) Ketones

A

A

82
Q

Which pathways are not stimulated by high levels of insulin?

A

any catabolic - ex. amino acid catabolism

83
Q

A novel signaling cascade is discovered that you suspect activates a G-αs subunit. What downstream events would be consistent with this discovery?

A

activation of adenylyl cyclase

84
Q

What is the primary oxidized fuel for skeletal muscle in the fasted state?

A

free fatty acids

85
Q

What is an insulin insensitive GLUT transporter found primarily on the liver?

A

glut 2

86
Q

Caffeine is a natural inhibitor of phosphodiesterase. If you were to consume a large amount of coffee you would likely see a prolonged response to which stimulants or hormones?

A

glucagon as inhibiting phosphodiesterase would increase concentrations of cAMP which is the second messenger for glucagon signaling

87
Q

A patient is found to have a rare disease in which the secretory function of the α-cells of the pancreas is impaired. As a consequence, glucagon cannot be secreted. Direct stimulation of which pathway in liver will be impaired?

A

gluconeogenesis - a fasted state pathway

Biochem (8 decks)

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