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Biochem > Week 4 > Flashcards

Week 4 Flashcards

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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
phosphatidylinositide metabolism
Gsq activates phospholipase C which cleaves PlP2 to form inositol-1,4,5-triphosphate and diacylglycerol
26
inositol-1,4,5-triphosphate
enhances Ca release from ER
27
diacylglycerol
activate protein kinase C
28
kinases catalyze
sequential transfer of Pi from ATP to hydroxyl groups to yield phosphatidylinositol-4,5-biphosphate
29
insulin in fed state
elevated
30
glucagon in fed state
low
31
cortisol in fed state
low
32
epinephrine in fed state
low
33
fuel for liver in fed state
glucose by glut 2
34
fuel for skeletal muscle in fed state
glucose by glut 4
35
fuel for RBC in fed state
glucose by glut 1
36
fuel for brain in fed state
glucose by glut 1 and 3
37
fuel for adipose in fed state
glucose by glut 4
38
insulin in fasted state
low
39
glucagon in fasted state
elevated
40
cortisol in fasted state
elevated
41
epinephrine in fasted state
elevated
42
fuel for liver in fasted state
free fa from lipolysis
43
fuel for skeletal muscle in fasted state
free fa from lipolysis
44
fuel for RBC in fasted state
glucose from hepatic gluconeogenesis and glycogenolysis
45
fuel for brain in fasted state
glucose from hepatic gluconeogenesis and glycogenolysis
46
fuel for adipose in fasted state
FA from store triacylglycerols
47
insulin in liver
``` glycolysis TCA glycogen synthesis FA synthesis protein synthesis ```
48
insulin in skeletal muscle
glucose uptake thorugh GLUT 4 protein synthesis glycogen synthesis
49
insulin in adipose
triacylglycerol synthesis | glucose uptake through GLUT4
50
glucagon in liver
glycogenolysis gluconeogenesis lipolysis beta-oxidation of FA
51
glucagon in skeletal muscle
no impact
52
glucagon in adipose
lipolysis
53
epi in liver
glycogenolysis via alpha agonist pathway lipolysis beta-oxidation of FA
54
epi in skeletal muscle
glycogenolysis via cAMP pathway
55
epi in adipose
lipolysis
56
cortisol in liver
enhances gluconeogenesis through enhanced transcription of proteins
57
cortisol in skeletal muscle
promotes protein catabolism to provide AA for gluconeogenesis occurring in liver
58
4 hormones controlling glucose homeostasis
insulin glucagon cortisol epinephrine
59
insulin signals through
receptor tyrosine kinase
60
glucagon signal through
G protein coupled receptor
61
cortisol signals through
binding an intracellular receptor
62
epinephrine signals through
ann additional g protein coupled receptor
63
insulin will increase the activity of
glycolysis glycogen synthesis fatty acid synthesis protein synthesis
64
when insulin increases glycolysis this
will generate pyruvate which is used to make acetyl coa which is oxidized in the TCA
65
glucagon leads to
- glycogenolysis - gluconeogenesis - release of stored TAG
66
supstrates for glucogenic processes come from
tissue proteins which are converted back into free amino acids and transaminated to carbon skeletons which are used to produce glucose
67
insulin signaling
- 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
docking of IP3 kinase on insulin receptor can
activate downstream kinase PDK1 or phosphoinositide dependent kinase
69
docking of grub 2 on insulin receptor can
activate map kinase cascade
70
primarily signal through g protein coupled receptors
epinephrine | glucagon
71
G alpha S activated
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
GQ subunit activate
phosphil APC which will cleave PIP2 into inositol triphosphate and diacylglycerol
73
diacylclycerol will
activate protein kinase C
74
IP3 will
enhance calcium release from the ER
75
``` 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
76
receptor for steroid hormones are
within cytosol or nucleus
77
primary fuel oxidized by tissues in fed state
glucose
78
glucose uptake in liver
glut2 transporter uptakes in insulin-independent manner - glut2 always present whether insulin is present or not
79
glucose uptake in skeletal muscle and adipose
insulin-dependent by glut4
80
glucose is oxidezed by
glycolysis
81
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
82
Which pathways are not stimulated by high levels of insulin?
any catabolic - ex. amino acid catabolism
83
A novel signaling cascade is discovered that you suspect activates a G-αs subunit. What downstream events would be consistent with this discovery?
activation of adenylyl cyclase
84
What is the primary oxidized fuel for skeletal muscle in the fasted state?
free fatty acids
85
What is an insulin insensitive GLUT transporter found primarily on the liver?
glut 2
86
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?
glucagon as inhibiting phosphodiesterase would increase concentrations of cAMP which is the second messenger for glucagon signaling
87
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?
gluconeogenesis - a fasted state pathway

Biochem (8 decks)

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