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EXAM 4 > Amino Acids > Flashcards

Amino Acids Flashcards

1
Q

insulin pathway

A

stimulates protein synthesis

insulin –>PKB/AKT –> P mTor –> P 4EBP –> can’t bind to eIF4E –> protein synthesis

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2
Q

glutamate decarboxylase

A

glutamate –> GABA

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3
Q

Creatine

A

Arginine, Glycine, SAM

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4
Q

Creatine Phosphate

A

Creatine (Creatine phosphokinase) Creatine Phosphate

Cretinine - normal amt excreted per day, used to calculate glomerular filtration rate

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5
Q

Kwashiokor

A

protein deficit

decreased muscle mass

distended belly

fatty liver - carbs make FA and esterify with glycerol, not enough protein for B100, decreased VLDL so FA hang in liver

a lot of liquid in abdomen - BP in blood vessels push fluid out, not enough protein in plasma for oncotic P - not normal P, pust BP out

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6
Q

Marasmus

A

E deficiency due to lack of calories

occurs earlier, better prognosis

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7
Q

N balance

A

N in = N out

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8
Q

+ N

A

N in > N out

anabolic - kids and adolescents

i.e. growth

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9
Q
  • N
A

N in < N out

catabolic

infection, severe trauma, wound healing

deficit of one or more essential AA

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10
Q

HPA axis

A

hypothalamus –> CRH –> pituitary –> ACTH –> adrenal gland –> cortisol –> protein degredation

cortisol (-) on ACTH and CRH

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11
Q

Cushing’s disease

A

excess ACTH

anterior pituitary adenoma

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12
Q

Cushing’s Syndrome

A

excess cortisol due to adrenocortical tumor

muscle wasting

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13
Q

Addison’s Disease

A

Deficit of Cortisol due to immune destruction of adrenal cortex

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14
Q

basic transamination rxn

A

AA donate N to a-keto-acid -

glutamate always one of the two AA-Alphaketoacid pairs

fulnneling of amino groups to glutamate

transaminases for all AA except lysine and threanine

need B6 for transaminases!!!

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15
Q

increased conentrations used to diagnose MI

A

alanine transaminase

aspartate transaminase

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16
Q

Glutamate dehydrogenase

A

glutamate –> alpha ketoglutarate

uses NAD(P)+ –> NAD(P)H

takes off amino group

free amonium ion

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17
Q

Trans-deamination

A

in the liver!!

  1. Transamination to glutamate - transaminases
  2. deamination of glutamate - glutamate dehydrogenase
  3. urea synthesis (in liver)

alpha keto acid is major E source for the liver

NH4 –> urea

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18
Q

Deamination by dehydration

A

serine –> serine dehydrotase –> pyruvae + NH4

threonine –> theronine dehydrotase –> alpha ketobutyrate + NH4

lose H2O, gain H2O

even if have transaminases, do this more!

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19
Q

hydrolytic deamination

A

gain h2o

glutamine –> glutaminase –> glutamate

asparagine –> asparaginase –> aspartate

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20
Q

direct deamination

A

histidine –> histidinase –> urocanate

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21
Q

purine nucleotide cycle

A

major generator of NH4+ in muscle

2ATP = ATP + AMP - use AMP to make more E

AMP –> IMP (lose NH3!! - fix to ammonium) –> + Asp adenylosuccinate –> Fumarate + AMP

Fumarate - goes to TCA, TCA cycle intermediate, allows active muschle to increase the size of the TCA cycle and generate more E

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22
Q

Glutamine Synthtase

A

Glutamate + ATP –> glutamine

ammonia fixation

23
Q

Ammonia fixation

A

uses free ammonium ion to make a covalent C-N bond

24
Q

First rxn of urea cycle

A

HCO3 + NH4 –> (carbamoyl P Synthetase I –> Carbamoyl P

N fixation

in mitochondria!!

N-acetyl glutamate is required activator!

Acetyl Co A + Glutamate (required Arginine activator) –> N-Acetyl Glutamate

Arginine is a signal that there is a lot of AA around (N)

25
Urea cycle
OCCAAFAU MITOC: Carbamoyl P + Ornithine --\> Citrulline CYTOSOL: Citrulline --\> Arginosuccinate --\> lose Fumarate --\> Arginine --\> lose Urea --\> Ornithine
26
benzoyl coA treatment
carbamoyl phosphate synthetase I or ornathine transcarbamolase benzoyl coA + glycine --\> hippurate (excrete) replace glycine via synthesis in the body and use NH3 -- decrease toxicity (phosphoserine transaminase) NH4+ is collected by glutamate dehydrogenase which by dransamination donates it to form glycine precursory - make more glycine and excrete it
27
phenylacetylglutamine synthesis
treatment for urea cycle deficiencies pre arginine conjugate to glutamine and excrete it in the urine amino acids donate N to glutamate - glutamate synthetase makes glutamine - glutamine is exceted - lose 2 N!
28
deficiencies of arginosuccinate synthetase and arginosuccinate
give arginine to restore ornithine
29
how glutamate uses N
transamination - transfers N from another AA glutamine dehydrogenase - fixes free NH3
30
ketogenic AA
leucine and lysine
31
glucogenic AA
all but leucine and lysine
32
glucogenic and ketogenic AA
PITTT phenylalanine isoleucine Tyrosine Threonine Tryptophan
33
Methionine Degredation
Methionine --\> SAM (lose CH3 - donate it to an acceptor) --\> SAH --\> homosysteine + adenosine Methionine is a major single carbon donor (methyl group) if methionine deficiency -- homocysteine is remethylated by B12 to become Methionine! (B12 is regenerated by N5-methyl-tetrahydrofolate!) if not - homosysteine + serine --\> cystathione --\> Cysteine + NH4 --\> alpha ketobutyrate --\> prioionyl CoA--\> syccinyl coA
34
Pellagra
vitamin deficiency lack of B3 int he diet decreased intake of niacin or tryptophan
35
B12 and Methionine Degredation
can't remake methionine required to make succinyl CoA - build up of precursors - neurotoxin!!
36
B6
required to convert homocysteine to crystathione increased homocysteine associated w increased risk of MI
37
Branched Chain AA Degrdation
mostly in extrahepatic!! much higher concentration different transaminase converts to alpha-keto-acid BUT branched-chain-alpha keto dehydrogenase is the same - increases with cortisol!! make acetyl CoA, propionyl coA, HMGCoA - enter TCA cycle transaminases are much higher in periphery need thiamin, niacin, riboflavin, patnothenate
38
Dehydrogenase components
E1 and E2 - specific for various R groups E3 is common - reoxidize the disulfide bonds
39
Maple Syrup Urine Disease
defects in any of the three components of branched chain alpha keto acids ketoacids build up - acidotic - severe neuro deficit always follw diet to prevent neuro damage
40
PKU
defect in phenylalanine hydroxylase phenylalanine + BH4 --\> tyrosine, dopa, doamine, norepi, epi build up - push to other pways Guthrie Card
41
alanine-glucose cycle
in muscle: glucose (glycolysis) --\> pyruvate --\> alanine (transamination) [alpha-keto-glutarate remade into glutamate by glutamate dehydrogenase) in liver: alanine --\> pyruvate by transamination transamination makes glutamate, NH4+ mad for glutamate dehydrogenase - urea! pyruvate made --\> glucose via glucoeogenesis - back to muscle
42
cortisol and alanine
cortisol induces alanine transaminase depresses AA transport into muscle/other extrahepatic tissue cortisol mobilizes AA from non hepatic tissue! transport AAs into hepatic tissue glucagon causes synthesis of increased alanine transporters in the liver
43
starvation
increased ketone bodies, decreased gluconeogenesis
44
stress
increased amino acid and cortisol --\> increase in branched-chain alpha keto acid dehydrogenase activity - more enters TCA cycle, makes alpha ketaglutarate --\> glutamate --\> glutamine (cortisol causes rise in muscle glutamine synthetase activity)
45
acidosis
glutamine - source of ammonia to buffer excess protons for excretion in the urine glutamine (glutaminase) glutamate (glutamate dehydrogenase) alpha ketoglutarate release 2 NH3+ transport as NH3 and H+ over membrane to glomerulus - recomibine and excete NH4 in urine increase glutamine production (increase muscle alpha keto acid dehydrogenase and muscle glutamine synthetase) decrease urea production from glutamine (decrease glutaminase in periportal cells of the liver) increase ammonia to buffer excess protons (activity of kidney glutaminase and glutamate dehydrogenase are increased)
46
alpha-keto-glutarate in the kidney - where does it go?
TCA cycle - malate to pyruvate to acetyl coA - reenter pyruvate to lactate pyruvate to oxaloacetate to PEP to glucose make alanine from glutamate and pyruvate (transamination) PEPCK - blood glucose level rises
47
cortisol mechanism
activates GR by binding and forming a dimer enter nucleus bind GRE transcribe PEPCK - increase blood glucose
48
AAs in acidosis
glutamine to kidney alanine to liver most others to the liver
49
AA in stress (not acidosis)
glutamine to tissues alanine to liver AA to liver
50
difolatereductase
2 NADPH Folate --\> FH4 add C to things
51
Sulfa Drugs
bacteriostatic - not bacteriocidal - time for immune system to respond prevent bacteria from dvisding in place of carboxyl group - inhibits reduction of folate
52
1 C Pool
Folate - can accept and donate C at different levels of oxidation most rxns of one C derviatives of FH4 are reversible
53
Folate Methyl Trap
irreversible rxn: N5N10 methylene FH4 --\> N5 methyl FH4 then donates CH3 to B12 to gen methionine from homocysteine in vitamin B12 deficiency - most folate in body is irrreversibly trapped as methyl derivative no supply of free FH4 to carry out rxns vitamin B12 def looks like folate def megaloblastic anemia - RBC increase in size but can't divide! can't undergo DNA synthesis (lack of thymidine and purines)
54
Methotrexate
competitive inhibitor of dihydrofolate reductase - used to treat cancer prevent cancer cells from DNA synthesis - cancer doing a lot of cell division kills a lot of other cells off and on

EXAM 4 (4 decks)

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