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part I > human metabolism: carbs, fats proteins (biochem) > Flashcards

human metabolism: carbs, fats proteins (biochem) Flashcards

1
Q

which is the only fuel that can be respired anaerobically?

A

carbohydrates

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2
Q

which 2 parts of body rely especially on carbohydrates?

A

brain

erythrocytes

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3
Q

monosaccharides examples x2

which foods are they found in?

A

glucose and fructose
(both found in fruit & honey)

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4
Q

disaccharides examples x2

what are their monosaccharide components?

which foods are they found in?

A

lactose (milk sugar)
glucose, galactose
milk

sucrose (table sugar)
glucose, fructose
cane sugar, prepared foods

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5
Q

trisaccharide (1)
what is its monosaccharide component?
which food is it found it?

A

trehalose

glucose

mushrooms

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6
Q

polysaccharides examples (3)

i) monosaccharide components
ii) foods they are found in

A

amylose
i) glucose (linear)
ii) plant starch

amylopectin
i) glucose (branched)
ii) plant starch

glycogen
i) glucose (branched)
ii) meat

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7
Q

what is the first stage of both aerobic and anaerobic respiration?

A

glycolysis

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8
Q

in which part of the cell does glycolysis occur?

what are the start and end products?

A

cytosol

glucose –> 2x pyruvate

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9
Q

under anaerobic conditions what happens to pyruvate?

which enzyme does this?

what other substance is involved in anaerobic respiration of pyruvate and what is it turned into?

A

reduced to lactate

lactate dehydrogenase

NADH –> NAD+

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10
Q

where does aerobic metabolism take place?

A

mitochondria

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11
Q

what is the cycle for aerobic respiration called?

A

tricarboxylic acid cycle (Krebs cycle)

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12
Q

what initially happens to pyruvate during aerobic respiration?

which enzyme catalyses this reaction?

what other substance is involved and what is it converted to/from?

A

pyruvate –> acteyl CoA + CO2

PDH (pyruvate dehydrogenase)

NAD+–> NADH

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13
Q

what happens to acetyle CoA in tricarboxylic acid acid?

A

acetyl CoA (C2) + oxaloacetate (C4)–> citrate (C6) –> cis-acetonate (C6) –> isocitrate (C6)

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14
Q

what happens to isocitrate in tricarboxylic acid cycle?

A

isocitrate (C6) –> a-ketoglutarate (C5) + CO2

NAD+–> NADH facilitates this reaction

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15
Q

what happens to a-ketogluterate (C5) in tricarboxylic acid cycle?

A

–> succinyl CoA (C4) + CO2

facilitated by NAD+ –> NADH

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16
Q

how does succinyl CoA become oxeloacetete in tricarboxylic acid cycle?

A

succinyl CoA –> succinate
facilitated by GDP –> GTP

succinate –> fumerate
facilitated by FAD–> FADH2

fumerate –> malate

malate –> oxaloacetate
facilitated by NAD+ –> NADH

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17
Q

products of each TCA cycle:

A

reduced co-factors: 3x NADH, 1x FADH2
high energy compound: 1x GTP
decarboxylation products: 2x CO2

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18
Q

how many moles of ATP are produces by:

i) aerobic respiration
ii) anaerobic respiration

A

i) 30-32
ii) 2

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19
Q

examples of partially anaerobic tissues: (4)

A
  • renal medulla
  • retinal cells
  • red blood cells
  • white (type 2) muscle fibres
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20
Q

white muscle fibres

  1. which fuel can they use?
  2. what do they store?
  3. what is storage product broken down to?
A
  1. only glucose
  2. glycogen

glycogen is broken down to glucose -1-phosphate then intermediate glucose-6-phosphate

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21
Q

how much glucose does the brain consume per day in:

i) fed state
ii) starved state

How quickly are glycogen stores used up in starvation?

A

i) 100g/day
ii) 25g/day

within 1st 24 hrs

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22
Q

how is glucose obtained during starvation?

A

breakdown of muscles

protein –> amino acid –> oxoacid

amino acid–> oxoacid
allows pyruvate –> alanine

alanine –> pyruvate in liver
which then allows for glucose production in the liver

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23
Q

what is the site of ketogenesis?

A

the liver

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24
Q

which transport molecule allows glucose to be taken up into brain?

A

GLUT 3

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25
Q

how is fat stored in the body?

A

triaglycerol (TAG/ triglyceride)

this forms lipid droplets in cytosol of adipocyte

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26
Q

major roles of fats in the body (5)
+ the form of fat involved in each

A
  1. energy storage
    - triglycerol
  2. membrane formation
    - phospholipids
  3. hormone synthesis
    - eicosanoids (prostaglandins, thromboxanes, leucotrienes formed from essential fatty acids)
  4. intracellular signalling
    - membrane phospholipids broken down to second messengers when hormone binds to its receptor
  5. regulation of gene transcription
    - fatty acids (+ fat-soluble vitamins)
27
Q

TAG (triaglycerol structure)

A

threecarbon glycerol backbone that is esterified to three
fatty acid side chains and the free fatty acid molecule constitutes the accessible energy source for cells and
tissues.

28
Q

which enzymes catalyses liberation of of fatty acid from TAG?

A

hormone-sensitive lipase (HSL)

29
Q

what affects HSL (hormonesensitive lipase) levels?

A

stimulated by:
- glucagon
- adrenaline
- noradrenaline

inhibited by:
- insulin
(HSL is elevated in diabetics due to poor insulin sensitiv/ porduction)

30
Q

how are fats transported in blood?

A

in protein complexes (as are hydrophobic and insoluble)

31
Q

Elevated levels of which one of LDL/ HDL can be sign of high fat diet?

A

LDL

32
Q

chylomicron
i. main fat constituent
ii. function

A

i. dietary TAG
ii. transports TAG from intestine to other tissues for oxidation or storage (fed state)

33
Q

VLDL (very low density lipoprotein)
i. main fat constituent
ii. function

A

i. endogenous TAG, cholesterol
ii. Transports TAG produced in the liver to other tissues where it can be oxidised (fasting state)

34
Q

LDL
i. main fat constituent
ii. function

A

i. cholesterol and cholesteryl ester
ii. transports cholesterol from liver to other tissues

35
Q

HDL
i. main fat constituent
ii. function

A

i. cholesteryl ester
ii. Scavenges cholesterol from many tissues and takes it to the liver for excretion

36
Q

fatty acid-albumin
i. main fat constituent
ii. function

A

i. fatty acid
ii. Transports fatty acids from adipose tissue to other tissues where they can be oxidised (fasting state)

37
Q

which 2 aerobic tissues consume and oxidise fatty acids at high rates?

A

heart tissue
red fibres of skeletal muscle

38
Q

name of pathway which oxidises fatty acids?

which part of cell does it occur in?

what are its products

diagram:

A

beta oxidation pathway

mitochondria

1x acetyl CoA
1x FADH2
1x NADH

39
Q

what is drawn to the liver to fuel gluconeogenesis during starvation?

A

oxaloacetate

40
Q

imbalance in of oxeloacete and acetyl CoA in liver during starvation

[liver takes up high levels of fatty acid so beta oxidation rates remain high resulting in an imbalance between CoA and oxeloacetate levles]

what does liver do with excess acetyl CoA?

A

ketogenesis

41
Q

how much of brain’s energy supply do ketones account for during starvation?

what level of ketones is sustained in body?

which is main ketone used for energy supply?

A

75%

8mmol/l

acetoacetane (acetone is what is excreted in urine)

42
Q

what elements are amino acids made from?

A

carbon
hydrogen
oxygen
nitrogen

43
Q

in amino acid breakdown what is disposed of separately from carbon skeleton?

why?

A

the amino group

to maintain nitrogen balance and prevent accumulation of toxic nitrogenous compounds such as ammonium ion (NH4+)

44
Q

what’s the first stage in amino acid metabolism?

A

removal of the amino group

45
Q

what happens in transamination?

which enzyme is involved?

A

amino group is transferred to a different carbon skeleton

a-ketogluerate –> glutamate

amino transferase

(remember is reversible in case NH4+ levels are low)

46
Q

what happens in de-amination?

enzyme involved

A

amino group is released as NH4+

glutamate +H2o–> a-ketoglutarate + NH4+

facilated by NAD+ –> NADH

glutamate dehydrogenase

(remember is reversible in case NH4+ levels are low)

NB. the pathway of amino acid degradation includes many aminotransferase enzymes with specificity for individual amino acids but only one enzyme (glutamate dehydrogenase) with deaminating activity

47
Q

urea cycle

  1. which organ does it occur in?
  2. which part of the cell?
  3. what is its purpose?
A
  1. liver
  2. mitochondria and cytosol
  3. detoxify ammonium to produce urea (non-toxic vehicle for transport of nitrogen out of body)
48
Q

upper limit of normal NH4+ in blood?

at what levels do sx of toxicity delevlop?

A

20 micromoles/ L (except for hepatic portal vein where concentrations are like 10x higher)

200 micromoles/L +

49
Q

urea cycle equation:

A

NH4+ + bicarbonate + asparte (amino acid) —> urea + fumerate (TCA intermediate)

facilitated by 3ATP –> 2ADP + AMP

50
Q

amino acids that are converted to which substance are ketogenic?

A

acetyl CoA

51
Q

which are the 2 main amino acids released by the brain during starvation?

what % of broken down amino acids do they account for?

A

alanine
glutamine

60-70%

52
Q

conversion of glucogenic amino acids to glucose

A
53
Q

phenylketonuria (PKU)

i. what is it?

ii. incidence in UK

iii. how many different polymorphisms account for this phenotype

A

i. absence/ greatly diminished activity of enzyme phenylalinase hydroxylase

ii. 1 in 10,000

iii. 300

54
Q

PKU what happens

A

i. acculumation of pheylalanine

interferes with uptake of other amino acids by competition with the saturable amino acid transporter

results in severe impact on developing brain

55
Q

screening test for PKU?

when is it done?

cut-off level for dx?

A

Guthrie test

6-14 days post natally

240 micromoles/L

56
Q

PKU mgt

A

exclude phenylalaline from diet but include tyrosine and other amino acids

must be followed strictly until 11 years

must be resumed in pregnancy

57
Q

which amino acid is phenylalanine closely linked to?

what appearance can this result in?

A

tyrosine

occulocutaneous albinism

58
Q

insulin sensitivity:
i. in early pregnancy vs normal
ii. in 3rd trimester vs normal

A

i. increased
ii. reduced by 50-70%

59
Q

TAG/ fatty acids in:
i. maternal tissues
ii. foetal tissues

A

i. deposition (early pregnancy)
oxidation and ketogenesis (later in pregnancy)
ii. little oxidate capacity, stored in late gestation

60
Q

glucose in:
i. maternal tissues
ii. foetal tissues

A

i. reduced insulin sensitivity so reduced uptake
ii. oxidised at high rates, staored as glycogen in late gestation

61
Q

amino acids:
i. in foetal tissues

A

consumed for proteins synthesis

62
Q

ketone bodies:
i. maternal tissues
ii. foetal tissues

A

i. higher circulating levels (indicate high ration of use)
ii. little if any oxidate capacity

63
Q

foetal metabolism

A

no gluconeogenesis initially as no glycogen stores in liver

fatty acid oxidation in liver ^^ post natally (but lipogenic capacity remains low until weaning)

64
Q

what else does neonate need dietry fat for (2)

A
  1. CNS development (3rd trimester to 3 months post natal)
    especially DHA, a derrivatiev of a-linoleic acid (an omega 3 fatty acid)
  2. thermogenesis
    - fatty acids are metabolised by brown adipose tissue for thermogenesis (infant does not have right muscles to shiver)

part I (12 decks)

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