lecture 5: amino acid metabolism 1 Flashcards

1
Q

why don’t amino acids have a storage form?

A

we can convert protein to ATP, still being used

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2
Q

protein turnover

A

synthesis and degradation of protein
influenced by factors such as oxidation

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3
Q

free amino acid pool remains constant

A

process that remove AAs = those that add amino acids
S + E = D + I
Positive nitrogen balance S > D
neg S < D
occur at equal rates S = D

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3
Q

how is excess nitrogen removed from the body?

A

AA breakdown removes nitrogen from body in the form of ammonia or urea
carbon skeletons remaining from removed N can enter TCA cycle

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4
Q

why would a protein turnover be required, even when the body requires no net gain or loss of protein?

A

replace proteins that have been oxidized, damaged, misfolded
adapt to new physiological and nutritional conditions (muscle breakdown - fasting state, starvation, illness)

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5
Q

which organs have higher protein turnover?

A

stomach, esophagus, colon - GI tract, replace epithelial lining
liver - metabolism

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6
Q

what individual proteins have higher turnover rates?

A

regulatory proteins - rapid adaptation of changing conditions

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7
Q

insulin in protein regulation

A

stimulates protein synthesis, inhibits protein degredation

insulin levels increase with feeding and decrease during fasting

signaling cascade > activation of mRNA translation

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8
Q

insulin protein synthesis activation mechanism

A

insulin or IGF-1 binds to receptor to stimulate Tyr phosphorylation of IRS-1

IRS-1 activation > stimulates kinases PI3K and pAKT

pAKT inactivates FoxO, which promotes protein breakdown, via phosphorylation > FoxO cannot enter nucleus

pAKT activates mTOR (promotes protein synthesis)

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9
Q

IRS-1

A

signaling adapter protein that plays a role in transmitting the signal from insulin to various kinases

activation > stimulates pAKT/PI3K

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10
Q

pAKT

A

kinase that inactivates FoxO, activates mTOR

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11
Q

FoxO

A

promotes expression of E3 ubiquitin ligases (genes involved in protein degradation), therefore promotes protein breakdown

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12
Q

mTOR

A

promotes protein synthesis

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13
Q

growth hormone (GH)

A

promotes longitudinal growth in adolescents
secreted by pituitary gland
initiates signal transduction that promotes expression of anabolic process genes

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14
Q

growth hormone anabolic cascade

A

GH binds to cell surface receptor, activates JAK2

JAK2 phosphorylates STAT proteins

phos. STAT proteins dimerize and enter nucleus

STAT proteins bind to specific DNA sequences, increasing expression (including IGF-1)

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15
Q

transcription factors

A

FoxO, STAT proteins
influence transcription process of various genes they regulate
enter the nucleus

16
Q

anabolic hormones in protein synthesis

A

insulin, IGF-1, GH

17
Q

catabolic hormones in protein degradation

A

glucagon, cortisol, myostatin

18
Q

glucagon

A

promotes gluconeogenesis from amino acids > not available for protein synthesis (redirection)

19
Q

cortisol

A

glucocorticoid hormone produced in the adrenal cortex
released in response to low glucose, stimulates gluconeogenesis

decrease protein synthesis and increase degredation

promote FoxO
inhibits eIF4 (initiates eukaryotic translation), therefore inhibiting synthesis

20
Q

myostatin

A

signaling molecule that inhibits the growth and differentiation of muscle cells, inducer of muscle wasting

inhibits insulin and IGF-1 signaling, mTOR effects

increases FoxO activity

21
Q

cytokines

A

peptides produced by cells of the immune system
reallocates muscle tissue to immune response

TNFa activates NF-kB > ubiquitin proteasome pathway

22
Q

inhibits protein synthesis

A

Y4E-BP, myostatin, glucagon, cortisol, TNFa/NF-kB

23
Q

promote protein synthesis

A

S6 kinase, eIF4 complex, mTOR, insulin, PI3K/pAKT, IRS-1, GH

24
Q

anabolic response to eating

A

insulin and AA supply > translation mRNA into protein
1) dephosphorylation of EIF2 > formation of pre-initiation complex
2) increased binding of eIF4 to mRNA

25
Q

fasting process

A

post-absorptive: insulin decreases, glucagon increases
early starvation: glycogen levels spent
long-term starvation: whole body protein degradation rates decrease > adipose depleted > protein degradation begins again

26
Q

exercise in protein synthesis

A

resistance exercise > mTOR signaling to promote S6 kinase and inhibit 4E-BP
4E-BP binds and inhibits eIF4 > prevents pre-initiation complex
mTOR inhibits 4E-BP
S6 kinase promotes pre-initiation complex