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Exam 1 > Metab 1-6, protein and lipids > Flashcards

Metab 1-6, protein and lipids Flashcards

1
Q

what is the 1st step in amino acid breakdown?

A

-NH2 removed by transamination or deamination and converted to urea to be excreted in urine

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2
Q

what happens to the carbon skeleton part of the amino acid that’s left over?

A

converted into different compounds to feed into other metabolic pathways

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3
Q

what are glucogenic amino acids?

A

feed into gluconeogenesis pathway to make glucose

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4
Q

what are ketogenic amino acids?

A

converted to acetyl CoA –> ketone bodies (via synthase to HMG CoA, then then via lyase to acetoacetate –> acetone)

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5
Q

what happens in transamination

A

-NH2 gets moved from an amino acid to a keto acid

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6
Q

what happens when a-ketoglutarate is the keto acid used? which enzyme is used?

A 
the addition of amino group (-NH2) to the a-ketoglutarate turns it into glutamate
alanine aminotransferase (ALT) is used for this reaction
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7
Q

what happens when oxaloacetate is used as the keto acid?

A

addition of NH2 will convert oxaloacetate to aspartate

enzyme used: aspartate aminotransferase (AST)

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8
Q

state the equation of alanine aminotransferase (ALT)

A

alanine + a-ketoglutarate pyruvate + glutamate

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9
Q

state the equation for aspartate aminotransferase (AST)

A

aspartate + a-ketoglutarate oxaloacetate + glutamate

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10
Q

what is deamination?

A

alternative pathway for removing amino group

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11
Q

what happens in deamination

A

amine group (NH2) removed from AA to form ammonia (NH3)

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12
Q

what are the effects of ammonia (NH3)?

A

very toxic
reduces TCA activity (depletion of substrate)
affects neurotransmitter synthesis

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13
Q

how do you get rid of NH3?

A

excreted in urine directly
can enter urea cycle to be excreted in urine
added to glutamate to make glutamine (safe N-store)

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14
Q

how is glutamine converted to glutamate?

A

glutamine –(glutaminase)–> glutamate + NH3

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15
Q

what happens to the produced glutamate?

A

glutamate a-ketoglutarate + NH4+

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16
Q

describe what happens in the urea cycle

A

converts ammonia into urea (soluble & inert - easy to excrete)
disposed as urine (kidney), converted to urea (liver)

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17
Q

where does the NH2 group of urea come from?

A

NH4+ (deaminate to NH3 and enter directly) or aspartate from oxaloacetate by transamination

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18
Q

what does defects in urea cycle cause? what do you treat with?

A

ammonia intoxication leading to tremors, slurred speech, blurred vision –> mental retardation (in children), seizures, coma
treat with low protein diet

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19
Q

what happens in phenylketonuria?

A

phenylalanine hydroxylase deficiency (phenyalanine –> tyrosine –> adrenaline etc.)
tyrosine is needed to make neurotransmitters & thyroid hormones (so becomes an essential AA)
PJU damages CNS, causing mental retardation

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20
Q

what happens in homocystinuria?

A

cystathionine ß-synthase (CBS) deficiency (requires vit B6)
homocysteine converted to methionine instead
cysteine is important for making proteins (fibrillin-1) in CT (so also affecting muscles, CNS, CVS)

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21
Q

how do you treat homocystinuria?

A

B6 supplements to help any remaining CBS get rid of homocysteine

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22
Q

What are the different lipids in the human body?

A

TAG (dietary lipid), phospholipids, ketones, cholesterols, vit ADEK

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23
Q

how are lipids stored? why

A

stored anhydrously in adipose tissue as they are hydrophobic

more energy than CHO as less reduced

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24
Q

what can lipids not be used in?

A

cells without itochondria e.g. RBCs or by CNS (can’t cross Blood Brain Barrier)

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25
Q

what are TAGs (from diet) broken down into and how?

A

broken down into 3 fatty acids + glycerol by pancreatic lipase in small intestines

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26
Q

what happens to the TAG once it’s broken down?

A

recombine into TAGs to be transported in chylomicrons to be stored in adipose tissues

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27
Q

how is TAG metabolism activated? inhibited?

A

by glucagon and adrenaline, inhibited by insulin

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28
Q

what happens to the glycerol and fatty acids once TAG is metabolised?

A

glycerol: enters glycolysis / gluconeogenesis

fatty acids: metabolised by liver, skeletal muscle, heart

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29
Q

How is fatty acid taken into correct location to be metabolised?

A

in mitochondria, too large to be transported across the mito membrane, so has to go through carnitine shuttle

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30
Q

Explain carnitine shuttle

A

fatty acid –(fatty acyl CoA synthase)–> fatty acyl CoA
carnitine + acyl CoA –(CAT1)–> CoA + acyl carnitine
acyl carnitine enters matrix
acyl carnitine + CoA –(CAT2)–> carnitine + acyl.CoA

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31
Q

once acyl.CoA is in the matrix, explain ß-oxidation

A

ß-oxidation oxidises FAs by repeatedly removing C2 molecules (acetyl) to combine to CoA to form acetyl CoA to enter TCA or synthesis of TAG or ketones

32
Q

what does ß-oxidation produce?

A

FADH2
NADH
all can enter oxidative phosphorylation

33
Q

how are ketone bodies produced?

A

acetyl CoA –(synthase)–> HMG CoA
HMG CoA –(HMG CoA reductase)–> cholesterol (INSULIN)
HMG CoA –(lyase)–> ketone bodies (GLUCAGON)

34
Q

where and when are ketones produced?

A

when the body is starving (low insulin:glucagon)

produced in the liver

35
Q

what are the normal ketone bodies value? in starved situation?

A

normal

36
Q

describe ketones

A

water soluble, so can be transported in the blood from liver –> tissues
converted back to acetyl CoA in muscle, heart & brain

37
Q

which organ can use ketones but doesn’t? why?

A

CNS can use ketones but ketone production means blood glucose concentrations are preserved for CNS

38
Q

What causes diabetic ketoacidosis?

A

high rate of ß-oxidation of fats in the liver as there is not insulin being produced (normally type 1) so fats are used instead of glucose as glucose is not taken up into cells

39
Q

Describe the formation of ketones

A

from fatty acids (from TAG) metabolism
fatty acid + CoA –(fatty acyl CoA synthase)–> fatty acyl CoA
fatty acyl CoA through carnitine shuttle into matrix using CAT 1 & 2 (acyl transported, there is CoA either side of matrix membrane
fatty acyl CoA –> acetyl CoA –(synthase)–> HMG (CoA) –(lyase)–> acetoacetate –> acetone

40
Q

what happens during diabetic ketoacidosis? (presenting diagnosis)

A

ketones present in urine

acetone is volatile and may be present in breath - breathed out and smelt

41
Q

What are the symptoms of diabetic ketoacidosis? what causes the symptoms?

A

hyperventilation, nausea, vomiting, dehydration, abdominal pain
caused by H+ ions associated with ketones producing metabolic acidosis (ketoacidosis)

42
Q

What is used in fatty acid synthesis?

A

uses energy from ATP
reduces FAD & NAD+ to FAD2H & NADH
input pf 2 CoA

43
Q

where does fatty acid synthesis take place?

A

in cytoplasm

acetyl CoA + oxaloacetate –> citrate to move from mitochondria to cytoplasm

44
Q

How are fatty acids build up? what does it use?

A

2 carbons at a time using fatty acid synthase complex

45
Q

Describe the process of fatty acid synthesis

A

acetyl CoA + CO2 –(acetyl CoA carboxylase)–> Malonyl CoA –(fatty acid synthase complex)–> 2 carbon atoms added to fatty A chain + CO2

46
Q

What controls how fast fatty acids are synthesised?

A

acetyl CoA carboxylase (to malonyl.CoA)

47
Q

aside from acetyl CoA carboxylase, what else regulates fatty acid synthesis?

A
  1. allosterically: high energy activate (citrate), low energy inhibits (AMP)
  2. covalent modification (adding / removing phosphate groups): insulin activates, glucagon/adrenaline inhibits
48
Q

What are the main energy stores in the body?

A

TAGs (15kg), muscle protein (6kg), glycogen (0.4kg)

49
Q

how do lipids travel around the body? why?

A

lipids are insoluble - need carriers
fatty acids bind to albumin
98% lipids are cholesterol (TAGs & cholesterol), so travel as lipoproteins

50
Q

what is the structure of lipoproteins?

A

sphere with surface coat (shell) of phospholipids, cholesterol & apoproteins
and hydrophobic core (TAGs & cholesterol esters)

51
Q

how do lipoproteins maintain their structure?

A

if spherical shape is maintained, dependent on ratio of core:surface lipids
lipids from hydrophobic core if taken up by cells then surface coat must also be reduced - by transfering to different particles or cell membrane
core can only be removed by lipases and transfer proteins

52
Q

what do chylomicrons transport?

A

DIETary TAGs from intestine to tissues e.g. adipose

53
Q

what do VLDLs transport

A

TAGs synthesised in liver to adipose for storage

54
Q

what do IDL transport?

A

short-lived precursor for LDL

transport of cholesterol SYNthesised in the liver to tissues

55
Q

What do LDL transport

A

cholesterol synthesised in liver to tissues

same as IDL

56
Q

what do HDL transport?

A

transport excess tissue cholesterol to liver for disposal as bile salts and to any cells requiring additional cholesterol

57
Q

which enzyme is responsible for removing core TAGs from lipoprotein particles? what up regulates this enzyme? how does it function?

A

lipoprotein lipase
found in inner surface of capillaries of adipose tissue & muscle
synthesis increased by insulin
lipoprotein lipase hydrolyses TAGs to release fatty acids and glycerol

58
Q

what happens to the fatty acid and glycerol hydrolysed by lipoprotein lipase?

A

fatty acids are taken up by tissues and glycerol transported to liver

59
Q

how is stability of the surface : core ratio restored?

A

when surface lipid is converted to core lipid
via enzyme LCAT
important in the formation of lipoprotein particles (maintaining structure)

60
Q

what does LCAT do?

A

converts cholesterol (surface) to cholesterol ester (core) using fatty acid derived from lecithin (phophatidylcholine)

61
Q

what does deficiency of LCAT lead to?

A

unstable lipoproteins of abnormal structure and a general failure in the lipid transport processes

62
Q

what is dyslipoporteinaemia?

A

any defect in the metabolism of the plasma lipoproteins

63
Q

What is hyperlipoproteinaemias?

A

raised levels of plasma lipoproteins

64
Q

what is type 1 dyslipoproteinaemia? (hyperlipoproteinaemia)

A

defective lipoprotein lipase

causing chylomicrons in fasting blood

65
Q

what is type 2a hyperlipoporteinaemia? what is it referred to as? associated risks?

A

defective LDL receptor
familial hypercholesterolaemia
raised LDLs in blood (as not taking up by cells) leading to increased risk of coronary artery disease (plaques building up)

66
Q

what are the signs of hypercholesterolemia?

A

xanthoma, xanthelasma, corneal arcus

67
Q

how do atheromas form?

A

endothelium damage leading to LDLs enter into blood vessel wall (now there is opening in endothelium)
LDLs become oxidised and then taken up by macrophages
macrophages become foam cells
foam cells accumulate to form plaques in vessel walls

68
Q

what can cause endothelial damage?

A

hyperlipidaemia, hypertension, smoking, toxins, haemodynamic factors, viruses, immune reactions

69
Q

what are the treatments of hyperlipoproteinaemias?

A

diet: reduce cholesterol, sat fats
lifestyle: increase exercise, reduce smoking
statins: inhibit HMG CoA reductase enzyme - decrease cholesterol production

70
Q

what are ROS and how are they formed?

A

during ox/phos by radiation or chemicals

O2 species with a single unpaired electron (highly reactive)

71
Q

what can ROS react with? what does it form?

A

react with lipids in cell membranes –> atherosclerosis
react with DNA to induce mutations
cause protein damage

72
Q

when can ROS be useful?

A

in WBCs to produce an oxidative burst to destroy bacteria

73
Q

how are superoxides formed? (O2.-)

A

during ox/phos - some electrons escape the ETC and bind only to oxygen
forming superoxide radical (O2 + e- –> O2.-)
unpaired electron make them highly reactive and damaging

74
Q

how is superoxide broken down? (to make it safe)

A

Superoxide –(Superoxide dismutase)–> hydrogen peroxide (H2O2)
H2O2 still a ROS
H2O2 –(catalase)–> H2O + O2

75
Q

how are hydroxyl radicals (.OH) produced and how do you get rid of them?

A

produced from H2O2 or radiation splitting H2O
v damaging, no enzymes to eliminate
need antioxidants to reduce them - glutathione (GSH) is the main antioxidant, so require NADPH to help free GSH

76
Q

what is the reaction between NADPH and glutathione?

A

GSH –(GSH peroxidase)–> H2O2 to H2O

GSSH –(GSH reductase)–> 2 x GSH (NADPH –> NADP)

77
Q

what happens to bile salts produced?

A

bile salts (deposition of excess cholesterol) bind to GI, causing more cholesterol to be broken down to form the bile salts that have been excreted / lost from binding to GI

Exam 1 (39 decks)

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