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

Metab 1-6, protein and lipids Flashcards

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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
what are TAGs (from diet) broken down into and how?
broken down into 3 fatty acids + glycerol by pancreatic lipase in small intestines
26
what happens to the TAG once it's broken down?
recombine into TAGs to be transported in chylomicrons to be stored in adipose tissues
27
how is TAG metabolism activated? inhibited?
by glucagon and adrenaline, inhibited by insulin
28
what happens to the glycerol and fatty acids once TAG is metabolised?
glycerol: enters glycolysis / gluconeogenesis | fatty acids: metabolised by liver, skeletal muscle, heart
29
How is fatty acid taken into correct location to be metabolised?
in mitochondria, too large to be transported across the mito membrane, so has to go through carnitine shuttle
30
Explain carnitine shuttle
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
31
once acyl.CoA is in the matrix, explain ß-oxidation
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
what does ß-oxidation produce?
FADH2 NADH all can enter oxidative phosphorylation
33
how are ketone bodies produced?
acetyl CoA --(synthase)--> HMG CoA HMG CoA --(HMG CoA reductase)--> cholesterol (INSULIN) HMG CoA --(lyase)--> ketone bodies (GLUCAGON)
34
where and when are ketones produced?
when the body is starving (low insulin:glucagon) | produced in the liver
35
what are the normal ketone bodies value? in starved situation?
normal
36
describe ketones
water soluble, so can be transported in the blood from liver --> tissues converted back to acetyl CoA in muscle, heart & brain
37
which organ can use ketones but doesn't? why?
CNS can use ketones but ketone production means blood glucose concentrations are preserved for CNS
38
What causes diabetic ketoacidosis?
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
Describe the formation of ketones
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
what happens during diabetic ketoacidosis? (presenting diagnosis)
ketones present in urine | acetone is volatile and may be present in breath - breathed out and smelt
41
What are the symptoms of diabetic ketoacidosis? what causes the symptoms?
hyperventilation, nausea, vomiting, dehydration, abdominal pain caused by H+ ions associated with ketones producing metabolic acidosis (ketoacidosis)
42
What is used in fatty acid synthesis?
uses energy from ATP reduces FAD & NAD+ to FAD2H & NADH input pf 2 CoA
43
where does fatty acid synthesis take place?
in cytoplasm | acetyl CoA + oxaloacetate --> citrate to move from mitochondria to cytoplasm
44
How are fatty acids build up? what does it use?
2 carbons at a time using fatty acid synthase complex
45
Describe the process of fatty acid synthesis
acetyl CoA + CO2 --(acetyl CoA carboxylase)--> Malonyl CoA --(fatty acid synthase complex)--> 2 carbon atoms added to fatty A chain + CO2
46
What controls how fast fatty acids are synthesised?
acetyl CoA carboxylase (to malonyl.CoA)
47
aside from acetyl CoA carboxylase, what else regulates fatty acid synthesis?
1. allosterically: high energy activate (citrate), low energy inhibits (AMP) 2. covalent modification (adding / removing phosphate groups): insulin activates, glucagon/adrenaline inhibits
48
What are the main energy stores in the body?
TAGs (15kg), muscle protein (6kg), glycogen (0.4kg)
49
how do lipids travel around the body? why?
lipids are insoluble - need carriers fatty acids bind to albumin 98% lipids are cholesterol (TAGs & cholesterol), so travel as lipoproteins
50
what is the structure of lipoproteins?
sphere with surface coat (shell) of phospholipids, cholesterol & apoproteins and hydrophobic core (TAGs & cholesterol esters)
51
how do lipoproteins maintain their structure?
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
what do chylomicrons transport?
DIETary TAGs from intestine to tissues e.g. adipose
53
what do VLDLs transport
TAGs synthesised in liver to adipose for storage
54
what do IDL transport?
short-lived precursor for LDL | transport of cholesterol SYNthesised in the liver to tissues
55
What do LDL transport
cholesterol synthesised in liver to tissues | same as IDL
56
what do HDL transport?
transport excess tissue cholesterol to liver for disposal as bile salts and to any cells requiring additional cholesterol
57
which enzyme is responsible for removing core TAGs from lipoprotein particles? what up regulates this enzyme? how does it function?
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
what happens to the fatty acid and glycerol hydrolysed by lipoprotein lipase?
fatty acids are taken up by tissues and glycerol transported to liver
59
how is stability of the surface : core ratio restored?
when surface lipid is converted to core lipid via enzyme LCAT important in the formation of lipoprotein particles (maintaining structure)
60
what does LCAT do?
converts cholesterol (surface) to cholesterol ester (core) using fatty acid derived from lecithin (phophatidylcholine)
61
what does deficiency of LCAT lead to?
unstable lipoproteins of abnormal structure and a general failure in the lipid transport processes
62
what is dyslipoporteinaemia?
any defect in the metabolism of the plasma lipoproteins
63
What is hyperlipoproteinaemias?
raised levels of plasma lipoproteins
64
what is type 1 dyslipoproteinaemia? (hyperlipoproteinaemia)
defective lipoprotein lipase | causing chylomicrons in fasting blood
65
what is type 2a hyperlipoporteinaemia? what is it referred to as? associated risks?
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
what are the signs of hypercholesterolemia?
xanthoma, xanthelasma, corneal arcus
67
how do atheromas form?
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
what can cause endothelial damage?
hyperlipidaemia, hypertension, smoking, toxins, haemodynamic factors, viruses, immune reactions
69
what are the treatments of hyperlipoproteinaemias?
diet: reduce cholesterol, sat fats lifestyle: increase exercise, reduce smoking statins: inhibit HMG CoA reductase enzyme - decrease cholesterol production
70
what are ROS and how are they formed?
during ox/phos by radiation or chemicals | O2 species with a single unpaired electron (highly reactive)
71
what can ROS react with? what does it form?
react with lipids in cell membranes --> atherosclerosis react with DNA to induce mutations cause protein damage
72
when can ROS be useful?
in WBCs to produce an oxidative burst to destroy bacteria
73
how are superoxides formed? (O2.-)
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
how is superoxide broken down? (to make it safe)
Superoxide --(Superoxide dismutase)--> hydrogen peroxide (H2O2) H2O2 still a ROS H2O2 --(catalase)--> H2O + O2
75
how are hydroxyl radicals (.OH) produced and how do you get rid of them?
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
what is the reaction between NADPH and glutathione?
GSH --(GSH peroxidase)--> H2O2 to H2O | GSSH --(GSH reductase)--> 2 x GSH (NADPH --> NADP)
77
what happens to bile salts produced?
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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