carbohydrate metabolism Flashcards

1
Q

what is metabolism

A

the process by which energy is derived from raw materials from food and used for growth and repair

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2
Q

explain the pathway of food

A

enters GI tract, is broken down and absorbed into blood where it can either be excreted or transferred to tissues where it is used for synthesis

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3
Q

what is a catabolic reaction

A

break down of larger molecules into smaller ones. this is an oxidative reaction where loss of H atoms occurs providing reducing power

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4
Q

what is an anabolic reaction

A

synthesis of larger molecules from building blocks using energy released from catabolic reactions. this is a reductive reaction because uses ATP and reductive poor from H atoms

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5
Q

what is required for the synthesis of new molecules

A

reducing power and energy

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6
Q

what is required for cellular process’ / cell function

A

energy

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7
Q

name the waste products of metabolism

A

CO2, H2O and (NH2)2CO (urea)

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8
Q

name the fuel molecules used during metabolism

A

building blocks used in biosynthesis e.g amino acids and these are used for growth and repair
organic precursors which allow interconversion of building blocks (acetyl coA)
biosynthetic reducing power (NADH)
energy(ATP)

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9
Q

types of work in the body which require ATP

A

biosynthetic
transport- ion gradients and transport of nutrients
specialised- e.g mechanical, electrical or osmotic

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10
Q

energy intake and energy consumption ratio of a healthy person

A

they are both equal

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11
Q

how much is 1kcal in kj

A

4.184KJ

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12
Q

which food sources contain the most and least energy

A

fat has most, then alcohol, then carbs and then protein has the least

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13
Q

what is energy used for

A

BMR- basal metabolic rate which is energy used each day is not moving = 1,400-1,700 kcal
activity- depends on how strenuous but = 1,000-3,000 kcal
specific dynamic action of food- this is the energy used to digest the food = 150kcal
some energy is also lost as heat

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14
Q

what happens when energy intake>use of energy

A

then synthesis or production of adipose tissue occurs

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15
Q

what happens when energy intake

A

then tissue will be lost

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16
Q

how long can you survive without food

A

20-70 days if average man or woman 70/58kg

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17
Q

what type of energy do cells use and why can’t they use heat energy

A

they use chemical bond energy. can’t use heat energy because man is isothermic and using heat would upset homeostasis

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18
Q

what is an exergonic and an endergonic reaction

A
exergonic= releases energy. delta G is less than 0 and occurs spontaneously 
endergonic= requires energy and delta G is more than 0. does not occur spontaneously
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19
Q

what is delta G

A

free standard energy change. is specific to a certain pH, temp and conc

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20
Q

what are the 2 redox reactions

A

oxidation = loss of e- or H atoms

OIL RIG

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21
Q

name the oxidised and reduced H carrier molecules

A
oxidised= NAD+, NADP+ and FAD 
reduced=NADH, NADPH and D=FADH2 - act as carriers for reducing power 
N= nicotinamide 
F= flavin 
A= adenine 
D= dinucleotide
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22
Q

what type of reaction is the break down of food

A

exergonic, this is the release of energy and an oxidation reaction. energy goes to NAD+ or NADP+ or FAD and energy is transferred for other uses e.g biosynthesis or ATP synthesis

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23
Q

NADH=

NADPH=

A
NADH= synthesis of ATP 
NADPH= biosynthesis
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24
Q

how is energy released from ATP

A

phosphate bond is broken releasing energy = exergonic

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25
Q

why is ATP a good energy molecule

A

it has high energy bona, it acts as a carrier and it is stable

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26
Q

name the high energy signals and what they do

A

ATP, NADH, NADPH and FADH2 they activate anabolic pathways

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27
Q

name the low energy signals and what they do

A

AMP, ADP, NAD+, NADP+ and FAD. - they activate catabolic reactions

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28
Q

what is creatine phosphate, how is it made and why do we need it

A

it is needed for when high energy needed quickly by some skeletal muscles. when lots of ATP is available then its used to make phosphocreatine and when there is low supply then its converted back releasing ATP simultaneously. the enzyme used is creatine kinase.

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29
Q

what is the enzyme ck used as a marker for

A

used as a marker for MI. it is released by myocardiocytes in blood after few hours

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30
Q

product of break down of creatine or phosphocreatine

A

creatinine

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31
Q

what is creatinine a marker of

A

used for measurement of muscle mass and measure hormones during pregnancy

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32
Q

what are the 4 main stages of catabolism

A

1) large molecules broken down in the gut and absorbed into the blood stream
2) metabolites are converted to acetyl coA and small amount of energy and reducing power are produced
3) Krebs cycle where more energy is released
4) ETC and oxidative phosphorylation where ATP is synthesised and lots of energy is released

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33
Q

what is a carbohydrates general formula and the types of carbohydrate

A
(CH2O)n 
mono- glucose, galactose and fructose 
di- maltose, lactose and sucrose 
olgi- dextrins
poly - starch and glycogen
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34
Q

for which cells is glucose a necessity

A

red blood cells, neutrophils, kidney medulla and lens of eye. also brain prefers glucose but will use ketone bodies in an emergency

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35
Q

stage 1 - break down in gut. give the details of the enzymes used

A

saliva- amylase which breaks down starch to olgisacherides
pancreas- amylase which breaks down starch/dextrins to mono
small intestine- lactase, sucrase and pancreatic amylase.
all broken down to monosacherides

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36
Q

why can’t cellulose be digested

A

because it has beta1,4 glycosidic bonds which we do not have an enzyme for to break it down

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37
Q

types of lactose intolerance

A

primary deficiency- absence of persistent allele meaning become lactose intolerance as get older. (when adult)
secondary deficiency- caused by injury to small intestine by disease e.g churns or coeliac. can be reversible
congenital- very rare. recessive deficient lactose gene where never have the correct lactase enzyme. can never digest milk even as baby

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38
Q

how are monosaccharides absorbed into the blood stream

A

1st absorbed from GI tract into intestinal epithelium by active transport by use of sodium pump
2nd absorbed from epithelial cell into blood stream by facilitated diffusion via the GLUT transporter

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39
Q

describe stage 2 in detail

A

this is the break down to produce acetyl coA and for carbohydrates this is called glycolysis. draw this out

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40
Q

enzymes and in the order they are used in in glycolysis

A

hexokinase.
phophofructokinase
pyruvate kinase

41
Q

features of glycolysis

A

2 net ATP produced by substrate level phosphorylation, NADH produced and glucose is oxidised (exergonic). this occurs in all tissues and is cytosolic

42
Q

why are there so many steps in glycolysis

A

easier, efficient energy consumption, allows fine control and interconnections between different pathways

43
Q

why are the steps using enzymes irreversible

A

because the delta G for the reverse reaction is not spontaneous

44
Q

what is the committing step

A

step 3. after this it is committed to glycolysis . before this can also be used for tother pathways

45
Q

clinical use of glucose

A

used in PET scan to diagnose cancer because cancer cells use lots of glucose yo because they have very high metabolism

46
Q

how is glycerol phosphate produced and what is it used for

A

it is produced from DHP in glycolysis and is catalysed by the enzyme G3P dehydrogenase and is used for the synthesis of triglycerides and phospholipids. production also results in production of NADH

47
Q

how is 2,3 bisphosphoglycerate produced and what is it used for

A

from 1,3 bisphosphoglycerate in glycolysis and is catalysed by the cyme bisphophosphate mutase. used in RBC for regulation of the release of O2 from haemoglobin

48
Q

what is lactate dehydrogenase and why do we need it

A

its an enzyme which catalyses the regeneration of NAD+ from NADH. in RBC (because no mitochondria for steps 3 and 4) and exercising skeletal muscles (incld brain GI and skin) NAD+ can not be regenerated and therefore glycolysis stops. lactase dehydrogenase catalyses pyruvate, NADH and H+ to form lactate and NAD+.

49
Q

how and where is lactate broken down

A

in heart and liver the reverse reaction is catalysed. in liver pyruvate is used for glucageneisis for more glycolysis and in heart its used for energy. done here because both these places are well oxygenated

50
Q

what is hyperlacteamia

A

high lactate. up to 5mM of lactate in blood but pH not yet raised because being buffered by proteins

51
Q

what is lactic acidosis

A

when enough lactate to reduce pH

52
Q

why does high lactate occur

A

either lots being produced or poor removal of it

53
Q

how is fructose metabolised

A

catalysed by fructokinase and aldose to produce 2 gylceraldheydes which are then able to join glycolysis

54
Q

what is essential fructosuria

A

fructokinase is missing which means there is fructose in urine but no clinical signs

55
Q

what is fructose intolerance

A

when aldose is missing meaning build up fructose1-P which can cause damage to liver meaning fructose. must be cut out of diet

56
Q

how is galactose metabolised

A

metabolised by galactokinase, G1P uridyl transferase and UDP galactose epimerase to form glucose which then joins glycolysis

57
Q

what is galactosaemia and what does it cause

A

when any 3 of the enzymes are deficient but if you are deficient G1P uridyl transferase or UDP galactose epimerase this results in the build up of galactose 1 P which then enters other pathways

58
Q

which other pathway does galactose 1 P enter and what happens

A

is converted to galacticol using up NADPH which is used in proper synthesis of sulphide bonds. if not present results in cataracs in lens or haemolysis from heinz bodies

59
Q

what is the pentose phosphate pathway

A

when glucose 6P is converted to ribulose which can still rejoin glycolysis and then ribose which is used in the synthesis of DNA, RNA and coenzymes. catalysed by enzyme G6P dehydrogenase.

60
Q

features of the pentose phosphate pathway

A

1) no ATP is produced
2) loss of CO2 means it is irreversible
3) production of NDAPH and therefore it is controlled by the ratios of NADP+ and NADPH
this means if this reaction is low then there will also be low NAPH and same problem as with galactosaemia

61
Q

types of allostery

A

1) binding to allosteric site to either inhibit or activate the enzyme
2) covalent activation whereby a phosphate group is added to enzyme altering the structure and causing either activation of inhibition of the enzyme

62
Q

why can irreversible steps be regulated and reversible ones cannot

A

because reversible means it will reach equilibrium and therefore not alter the amount of product. irreversible reaction cannot equilibrate

63
Q

explain allosteric regulation by the product

A

the product reduces the entry of the substrate and therefore the build up of intermediates. this is called feedback inhibition

64
Q

what is the committing step and why is it a good target for regulation

A

committing step means substrate can no longer be directed to other pathways. this means by inhibiting this pathway the substrate will be sent to other pathways

65
Q

which molecules inhibit or activate enzymes

A

high energy will inhibit enzymes and low energy will activate enzymes

66
Q

explain hormonal regulation

A

hormone will bind to the receptor and activate a signalling pathway and this will activate a protein kinase or protein phosphatase which will either phosphorylate or dephosphorylate an enzyme altering the activity of the enzyme

67
Q

what is feedforward regulation

A

early pathway substrate provides signal to stimulate later enzyme to activate a pathway

68
Q

adrenaline as an example of phosphoregulation

A

adrenaline activates protein kinase A which activates a kinase activity an enzyme which promotes glycogen break down

69
Q

insulin an an example of phosphoregulation

A

dephosphorylation of an enzyme will stimulate glucose use and of another enzyme will inhibit glycogen break down

70
Q

how is hexokinase in glycolysis regulated

A

regulated by product inhibition by G6P

71
Q

how is PFK regulated in glycolysis

A

high [ATP] inhibits PFK and high [AMP] will stimulate PFK. also high insulin concentrations stimulated PFK in order to make use of the glucose

72
Q

how is step 6 (the NADH one) regulated in glycolysis

A

is regulated by conc ratios of NADH/NAD+. when [NADH] is high then there is inhibition of step 6

73
Q

how is pyruvate kinase regulated

A

it is stimulated by high insulin

74
Q

what happens before pyruvate enters the Krebs cycle

A

pyruvate is converted to acetyl coA by pyruvate dehydrogenase. CO2 is produced and is therefore an irreversible reaction meaning is a key regulatory step

75
Q

equation for the conversion of pyruvate to acetyl coA

A

pyruvate + coA + NAD+ = acetylcoA + CO2 + NADH +NAD+

76
Q

how is the pyruvate dehydrogenase regulated

A

it is activated by NAD+, ADP and insulin and inhibited by NADH, ATP citrate and acetyl co A

77
Q

key features of the Krebs cycle

A

it occurs in the mitochondria , require fad and nad+, produces some energy and biosynthesis precursors e.g amino acids, fatty acids and heat groups as well as glucose DRAW IT OUT

78
Q

hw many FADH2, NADH and GTP per molecule of glucose produced by the TCA cycle

A

2 FADH2, 6NADH and 2 GTP

79
Q

during the TCA cycle which bonds are broken and what conditions are required

A

requires O2 for function. all c-c bonds and c-h bonds are broken during the Krebs cycle. c atoms are also oxidised to form co2. all H atoms are transferred to H carrier moelcules

80
Q

how many total ATP produced at end of Krebs and where is the rest of the energy

A

4 ATP rest of ATP synthesis occurs in mitochondria by the ETC. lots of energy is produced ad needs O2 to function as it acts as the final electron acceptor. draw structure of mitochondria

81
Q

explain the ETC and how it works

A

NADH and FADH2 are oxidised by enzymes and the electrons are transferred along the electron transport chain each time releasing energy which is used to pump H+ ions out of the inner membrane space into the mitochondria

82
Q

relative electron energy between FADH2 and NADH

A

NADH electrons have more energy. 2.5 ATP per NADH and 1.5 ATP per FADH2

83
Q

how is ATP synthesised

A

H+ move back into intermembrane space down their electrochemical gradient and ATP is synthesised by the enzyme ATP synthase

84
Q

how is the ETC regulated

A

when [ATP] is high [ADP] is low and therefore there is no substrate for ATP synthase meaning H+ stops flowing into mitochondria and H+ conc in inter membrane space increases preventing H+ being pumped out. NO MORE ATP

85
Q

how is the TCA cycle regulated

A

isocitrate dehydrogenase which catalyses isocitrate is activated by ADP and inhibited by NADH and ATP
alpha ketogluterate dehydrog is inhibited by NADH and ATP and succinylcholine coA which is the product. (this is from c5 to c4)

86
Q

inhibitors of the ETC

A

e.g cyanide prevents oxygen from accepting the electrons therefore preventing the ETC from continuing and therefore stop ATP synthesis

87
Q

what are uncouplers

A

uncouplers increase the permeability of the innermemrbane to protons reducing proton gradient (p.m.f). an example of an uncoupler in fatty acids

88
Q

diseases that affect ATP synthesis

A

if issue with mtDNA then no ETC and no ATP synthesis

89
Q

what is energy coupling and how is this controlled in brown adipose tissue

A

it is how efficiently the energy from the ETC is converted for ATP synthesis. rest is lost as heat. more tightly bound = more energy. in brown adipose tissue uncouplers (fatty acids) callow extra heat to be released by the enzyme thermogenin

90
Q

explain how thermogenin works

A

fatty acids activate thermogenin and make it transport H+ back into mitochondria. ETC is uncoupled fro ATP synthesis and energy from p.m.f is relased as heat

91
Q

where is brown adipose found and why is it needed

A

extra heat needed in new horns and hibernating animals

92
Q

oxidative phosphorylation vs substrate level phosphorylation

A

OP- occurs in mitochondria, requires O2, los of ATP produced, energy coupling is indirect via ETC and ATP synthesis (p.m.f)
SLP- occurs in mitochondria and in cytoplasm, no O2, barely any ATP produced, energy coupling via P group transfer onto ATP.

93
Q

how many ATP molecules are produced from 1 glucose molecule

A

32 ATP

94
Q

what is marasmus

A

occurs due to insufficient energy intake due to multiple nutritional deficiencies. This is due to protein being used for energy in the brain and therefore loss of muscle protein

95
Q

appearance of marasmus

A

very thin limbs and very underweight.

96
Q

side effects of marasmus

A

unable to replace and repair tissues therefore GI tract is affected, anaemia develops, hormones affects and the cardiovascular system is impaired. the brain is also affected in severe forms

97
Q

what is kwashiorkor

A

calorie intake is normal but have very low protein intake. need essential amino acids from the diet for synthesis of some essential proteins. liver therefore cannot use proteins to make lipoproteins and fatty acids will build up in liver causing septic disfunction and oedema occurs due to reduced onctoic pressure of plasma causing fluid to move out of plasma

98
Q

appearance of kwashiorkor

A

swelled legs and pot belly. thin muscles but fat present

99
Q

what is re feeding syndrome

A

ammonia toxicity due to down regulation of enzymes in urea cycle meaning can’t digest proteins. must reintroduce very slowly.