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Foundations 1 > Week 3 Amino Acid Metabolism Nitrogen Balance Module > Flashcards

Week 3 Amino Acid Metabolism Nitrogen Balance Module Flashcards

1
Q

of the 20 AA how many can be generated by the bodY

A

11

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2
Q

protein accounts for what % of nitrogen in body?

A

95%

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3
Q

how are lipids stored int he body?

A

adipose tissue

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4
Q

how is glucose stored in the body?

A

glycogen (liver, muscle)

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5
Q

how is protein stored in the body?

A

its not!

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6
Q

what are the three states of nitrogen balance?

A

negative, positive, equilibrium

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7
Q

what is a negative nitrogen balance?

A

inadequate nitrogen intake or hyper-catabolic state

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8
Q

what is positive nitrogen balance?

A

a person is accumulating protein in the body over what is needed to maintain lean body mass (ideal for growing children)

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9
Q

what is the free amino acid pool?

A

ALL free amino acids of the body. those present in all tissues including blood.

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10
Q

what are the pathways that deplete the free amino acid pool (3)?

A

protein translation, nitrogenous compound biosynthesis, amino acid catabolism

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11
Q

what are the pathways that maintain the amino acid pool?

A

degradation of body proteins, dietary amino acids, biosynthesis of non-essential AA

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12
Q

what is the largest compartment of amino acids?

A

body proteins

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13
Q

what is protein turn over?

A

refers to the total flux (in and out) of proteins through protein synthesis and protein degradation pathways

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14
Q

how does lean tissue deposition occur?

A

protein synthesis>protein degradation

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15
Q

how does lean tissue wasting occur?

A

protein degradation>protein synthesis

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16
Q

which amino acids can be converted to purines and pyrimidines? 3

A

Gly, Asp, Gln

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17
Q

Along with Pur and Pyr, Gly is also a precursor for what to molecules?

A

heme and creatine

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18
Q

what neurotransmitters origanate from the free AA pool?

A

serotonin (Trp), GABA (Gln), histamine (His), EP, NE (Tyr)

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19
Q

NO is made from what AA

A

Arg

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20
Q

when the body degrades amino acids, what occurs to the N?

A

excreted in urine

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21
Q

what is the significance of N being excreted in the urine?

A

gives us a window to body protein homeostasis

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22
Q

nitrogen equilibrium exists when

A

nitrogen intake= excretion

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23
Q

when we have a positive nitrogen balance?…what state is the body in

A

intake>excretion and the protein compartment grows. anabolic state

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24
Q

when is positive nitrogen balance required?

A

in normal growth, (supports gains in lean body mass)

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25
Q

what is a negative nitrogen balance? what state?

A

excretion>intake. catabolic state

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26
Q

when the body is in a negative nitrogen balance how is free amino acid pool maintained?

A

proteins are degraded

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27
Q

which compartment (amino acid pool or body protein) is maintained within a narrow compartment

A

amino acid pool! the pathways that add to it and take from it are narrowly regulated

28
Q

nitrogen balance is measured by….

A

nitrogen ingested-nitrogen excreted

29
Q

what is a non-nutritional cause of negative nitrogen balance

A

cachexia

30
Q

what is cachexia? cause? seen in? treatment?

A

a hyper-catabolic state. results in profound weight loss. seen in cancer, chronic renal disease, severe burns. Treat: stimulate anabolism (steroids)

31
Q

anabolism:

A

building

32
Q

catbolism

A

breaking down

33
Q

what do anabolic steroids do to nitrogen balance?

A

lead to a large increase in nitrogen balance where less nitrogen is being excreted. build protein (and muscle)

34
Q

most of the body protein is in…

A

skeletal muscle (40%)

35
Q

if a decrease in dietary protein does not explain cachexia, what does?

A

the inflammatory response. cytokines catabolize skeletal muscle causing an influx in the AA pool and a correlated increase in AA breakdown

36
Q

why are some AA ‘essential’?

A

out body doesnt have the machinery to produce them. Probably an evolutionary thing that resulted in us conserving energy by eliminating the need to synthesize some of the more metabolically complex AA

37
Q

compared to essential AA, the number of proteins needed to make non-essential AA is….

A

far less. Essential AA would require an average of 6.6 additional enzymes per AA

38
Q

why are Tyr and Cys conditionally non-essential?

A

they can be synthesized from the essential Phe and Met

39
Q

the N equilibrium is determined mainly by…

A

the most limiting AA (essential), the N equilibrium point will differ for protein sources of different quality

40
Q

what is an incomplete protien?

A

protein that does not provide all the essential AA

41
Q

what does a nitrogen balance curve look like for incomplete proteins?

A

smaller slope and larger x-intercept

42
Q

where is nitrogen equilibrium on a nitrogen balance curve?

A

the x-intercept

43
Q

all non-essential AA except Tyr and Cys can be synthesize by…

A

transamination from Glutamate

44
Q

Phe+Phe hydroxylase–>

A

Tyr

45
Q

a deficiency in Phenylalanine hydroxylase results in…

A

phenylketonuria (PKU)

46
Q

what is the cofactor of Phe hydroxylase?

A

tetrahydrobiopterin

47
Q

co factor

A

a molecule essential of enzyme function

48
Q

Phe hydroxylase deficiency can be caused by which two things?

A

mutation in gene encoding Phe hydroxylase or an inability to regenerate tetrahydrobiopterin

49
Q

why is Phe hydroxylase deficiency a problem? (2)

A

its product (Tyr) becomes an essential AA along with its downstream metabolites. Also, an increase in the reactant (Phe) leads to the accumulation of neurotoxic metabolites of phenyllactate and phenylacetate

50
Q

what is the therapy for PKU?

A

suppmlment Tyr and avoid Phe (things that contain aspartame such as artificial sweeteners)

51
Q

how is the (conditionally) non-essential AA Cys produced?

A

in two steps from the non-essential AA Ser with the help of the essential AA Met

52
Q

How does Met contribute to Cys synthesis

A

donates its sulfur, through its metabolite homocysteine (these are the only two sulfur containing AA)

53
Q

what is homocystinuria? cause?

A

rare recessive disorder caused by a mutation in the gene coding for cystathionine synthase (CBS)

54
Q

what is the role of CBS?

A

role in producing Cys from Met and Ser

55
Q

what accumulates in people with homocystinuria? why is this bad?

A

Met, homocysteine. homocysteine disrupts collagen cross-linking and leads to premature atherosclerosis, strokes, heart attacks, and mental retardation

56
Q

how is homocystinuria treated?

A

diet: limit Met and supplement Cys

57
Q

what is cystathioninuria?

A

a disorder in which cystathionine (metabolite of homocystein) accumulates. relatively benign because this intermediate doesnt feed into many pathways

58
Q

how is Asn (non-essential) asparagine produced? enzyme

A

in a single step from aspartate (Asp) with the enzyme asparagine synthetase (requires ATP)

59
Q

what is the cause of acute lympahtic leukemia?

A

Asparagine snythetase deficiency in WBCs. Asn can’t be produced and becomes essential AA

60
Q

what is the treatment for acute lymphatic leukemia?

A

administration of L-asparaginase (enzyme in prokaryotes that converts Asn TO Asp) that depletes Asn and kills cancerous leukocytes

61
Q

how is glutamine (Gln) produced?

A

in a single step from Glu and ammonia by the enzyme glutamine synthetase (requires ATP)

62
Q

what is the most abundant AA

A

Gln

63
Q

What can be said about Gln transfer among organs

A

it is the FASTEST making Gln a major vehicle in N transfer among tissues

64
Q

Cachexia also depletes what AA (along with protein)?

A

Gln, therefore supplementing Gln is used to treat Cachexia

65
Q

what are important conditions that require a positive nitrogen balance?

A

pregnancy and childhood growth

66
Q

what are two causes of a negative nitrogen balance?

A

malnutrition, cachexia

Foundations 1 (65 decks)

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