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cholesterol > bile aicds and cholesterol > Flashcards

bile aicds and cholesterol Flashcards

1
Q

primary bile acids

A

cholic acid

chenodeoxycholicacid

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2
Q

secondary bile acids and how do we form them

A

Deoxycholic acid
lithocholic acid

formed from primary after dehydroxylation by intestinal bacteria

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3
Q

how are bile acids made

A

cholesterol goes to the liver and gets degraded to the bile acids. Need 17 enzymes to make bile acids. l key enzyme 7 a hydroxylase which needs o2 NADPH, cytp450 vitamin c it makes 7 a hydroxycholesterol which is where bile acid synthesis starts

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4
Q

what route can primary acids take

A
  1. converted to 2 acids
  2. be conjugated in peroxisomes with glycine or taurine/glycoconjucgates and tauroconjugates
    cholic acid- glycocolic acid + taurocholic acid
    chenodeoxycholic- glycocheonodeoxycholic acid and tarochenodeoxycholic acid
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5
Q

why do we conjugate bile acids

A

because more amphipathic (better emuslifier) and more easily secretable and less cytotoxic

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6
Q

propterties of bile and contents

A

emuslification
neutralization of acid
excretion

phospholipids
bile acids
cholesterol
bilirubin

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7
Q

hepatic bile and gall bladder bill

A

gall bladder bile is more concentrated, more dense

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8
Q

7 a hydroxylase

7 a dehydroxylase

A
  1. the common precursor for bile acids

2. intestinal bacteria to form secondary bile

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9
Q

regulation of bile acid synthesis

A

7 a hydroxylase , regulated by covalent modification, enzyme is active in its phosphorylated form unlike HMG - CO reductase which makes cholesterol and this makes sense! also the product which is bile acids negatively inhibits the enzyme and cholesterol which is the precursor for bile acid synthesis stimulates the enzyme!

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10
Q

functions of bile acids

A
  1. represent the only significant mechanism feces represent the only significant mechanism for the elimination of excess cholesterol

They facilitate the digestion of dietary hey facilitate the digestion of dietary
triacylglycerols by acting as triacylglycerols by acting as emulsifying agents emulsifying agents that
make fats accessible to fats accessible to pancreatic lipases pancreatic lipases.

allow for the absorption of fat soluble vitamins

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11
Q

what is a bile salt

A

it is the k and Na salts of the conjugated bile acids

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12
Q

enterohepatic circulation

A

the majority of the bile gets reabsorbed back int he terminal ileum via the enetrehepatic circulation from there it will go back to the liver. only a small fraction scape and is eliminated with he faeces

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13
Q

clinical symptoms -

A

cholelithiasis - gall stones. where there is too much cholesterol in bile, bile becomes supersaturated with cholsetrol so cholesterol precipitates out of the bile.

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14
Q

cholesterol is a precursor for

A

bile salts
vitamin D
steroid hormones - gluccocroticoids,mineralcorticoids,androgens,estrogens

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15
Q

what do esterases do

A

break down cholesterol esters

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16
Q

regulatory enzyme for cholesterol synthesis

A

HMG CO A R. active in its dephosphorolated form (opposite to 7 a hydroxylase which makes sense because they are reciprocal processes)
:) insulin + thyroid homrones
:(cholesterol - product
:(bile acids
:(statins- as statins want to reduce cholesterol

:( glucagon + gluccocorticoids -camp pathway

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17
Q

how do we eliminate cholesterol from the body

A

as free cholesterol or as bile acids 1g a day 0.5 g each

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18
Q

main places of cholesterol synthesis

A

gonads-testes n ovaries
adrenal glands
liver

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19
Q

CM
LDL
HDL

A

CM: transports chol to the liver

takes TAG from diet to tissues via lacteals starts of as nascent before it has it apo proteins then HDL gives it C2 and E making it mature.now CM can deposit Tag to cells by lipoprotein lipase (found in the walls of blood v). LPL needs C2 to become active

LDL: B cholesterol made by liver and sent to the cell (same with VLDL). The cells have an LDL receptor of which the ldl gets internalised by recepotor mediated enedocytosis and then lysosomes hydrolyse- inside relaeasing choleterol

HDL: A cholesterl

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20
Q

ACAT

A

acylcoA cholesterol acyl transferase makes cholesterol esters (FFAS) so that can form lipoprotein

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21
Q

values of choleterol

A

normal range 3.7-5.7 mmol

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22
Q

framingham study

A

found that 70% men with CHD had less than 1 mmol of HDL choletserol shows that the highter the HDL the lesser the risk

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23
Q

effects of increased choletserol

A 
diabetes
obesity
arthersocelerosis
hypofucntion of thyroid gland 
hyperfunction of adrenal gland (crushings disease)
early stage of liver damage
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24
Q

decreased choletserol

A 
stravation
hyperfucntion of thryoid gland
hypofunction of adrenal gland
final stages of liver damage
colitis
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25
Q

Role of LCAT

A

Associated with HDL, responible for the transport and elimination of choletserol from the body. HDL removes cholesterol from extrahepatici tissued and esterfies it using LCAT, then taken up by the liver after binding with HDL receptor. The cholesterol can be used to make bile salts or new lipoproteins

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26
Q

HDL receptor

A

apo A1

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27
Q

LDL receptor

A

B100

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28
Q

What happens if LDL is in excess

A

then scavenger cells (macrophages) oxidise LDL (oxiLDL) and become foam cells which contribute to development of arteriosclerosis

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29
Q

Which part of the cell do we make choletserol

A

cytoplasm then continues in the EPR

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30
Q

What effect does increased concentrations of choletserol have

A
  1. inhibits the endogenic synthesis fo cholesterol (HMG -COA R)
  2. decreased denovo synthesis of LDL receptors
  3. stimulation of enzyme that makes cholesterol esters (ACAT)
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31
Q

Wat is the substate for cholesterol syntehesis and where does it come from

A

acetyl coa comes from degradation of carbohydrates (krebs)

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32
Q

what do we need to make cholesterol

A

because its an anabolic process, reuires a lot of ATP and NADPH

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33
Q

what do statins do

A

structural anaologs of HMG COA decrease B cholesterol and TAG and increase a cholesterol. side effects myopathy

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34
Q

what drugs affect cholesterol levels

A

statins- tructural anaologs of HMG COA decrease B cholesterol and TAG and increase a cholesterol. side effects myopathy

bile acid sequestrants _ they bind to intestinal bile acids preventing their reabsorption thus eliminating cholesterol
side effects: they can increase TAG levels
GI distress
constipation

pharmocological doses of niacin b3
-decrease LDL
-increase HDL
side effects : GI distress, hyperglycemia, hepatotoxicity

Fibric acids
-decrease LDL increase HDL
mechanismof action: increase LPL activity
SE: gall stone

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35
Q

what stimulates fatty acid synthesis

A

when you have an excess of calories (glucose) but also an excess of proteins can also increase FA.

36
Q

define the terms
lipolysis
B oxidation
Lipigenesis

A

ll: breaking down TAH

BO: breaking down fatty acids

lipogensisi: making FA

37
Q

Where does lipogeneis occure

A

mainly liver but can occur in adipose tissue, kidney,brain and mammary gland

38
Q

compariosn of FA synthesis and FA breakdown

A 
Synthesis:
cytosol
NADPH
multienzyme complex -FAS
2 carbon units re joined to be converted to malonyl coA
breakdown:
mirochondria 
NAD +FAD
independant enzymes
releasing of 2 c unit
39
Q

regualotry enzyme of Fatty acid synthesis

A 
Acetyl coa carboxylase
irreversible step + commited step  
because its a carboxylase it requires biotin, ATP and carbon source (co2 or HCO3)
\:) acetyl Coa
\:) citrate 
\:) ATP
\:(palmitoyl

activated in its dephopshorlated form (similar to HMG - COA R)

40
Q

Where does the NADPH come from for fatty acid synthesis

A

PPP
but also oxaloacetate can be used to generate NADPH because the reverse reaction of TCA cycle occurs using malate DH. NAD is produced and malate which is a substarte for Malic enzyme which makes NADPH!

41
Q

fas complex

A

multienzyme complex composed of 2 identical subunits
each subunit has 7 catalytic sites and 1 ACP

The ACP contains a 4’ phosphopantethein residue

The two subunits are associate in a head-to-tail
arrangement, so that the ACP sulfhydryl group on
one subunit and a cysteinyl sulfhydryl group on
another subunit are closely aligned.

42
Q

What conditions favour FA synthesis

A
  • high levels of citrate

- high levels of ATP

43
Q

describe and draw how FAS synthase

A

FAS has a cystein-sh group (above) and an ACP - sh below. Acetyl moiety gets transfered to the ACP part and then to the cyst part (temporary holding group)

malonyl moiety comes and binds to the ACP part

malonyl + acetyl condense with the release of co2 whcih comes from malonyl

sequence happens 7 times until a staurated 16 c palmitoyl has been formed. this is liberated from the enzyme complex by thiosterase to produce palmitate which will then be converted to palmitoyl COA

44
Q

elongation of fatty acids

A 
1. EPR
microsomal system
donar: malonyl coa
reductant is NADPH
basically picks up where FAS left off because its limit is 16 c
  1. Mitochondria ( minor process)
    -reversal of B oxidation
    donor: acetyl COA
    reductant NADH
45
Q

How many C does palmitoyl have

A

16c

46
Q

energetic balance

A

synthesis of palmitoyl needs 7 cycles
each cycle 2 NADPHS
8 moles of Acetyl coa + 8 ATps

47
Q

regulation of lipogenesis

A

the main regulatory factor is the nutritional state of the organism. rate is high on a high CARB diet and low fatty acids.

ihibition: fatty diet, deficiency of insulin (because insulin stimulates FA synethesis)

2 regulatory enzyymes, main one acetyl coa caboxylase and then FAS

48
Q

enzymes involved in Fatty acid synthesis

and scheme

A
  1. acetyl transacylase
  2. malonyl transacylase
  3. ketoacyl synthase
  4. ketoacyl reductase-NADPH
  5. hydratase
  6. enoyl reductase
  7. thioesterase
49
Q

name ketone bodies and structures

A
  1. acetacetate
  2. acetone
  3. B hydorxybutyrate
50
Q

how do we form kb

A

when we have high levels of B oxidation

51
Q

where does Kb formation take place

A

mitochondria liver

52
Q

normal concentratio of KB

A

less than 2 mmol

53
Q

the ocnversion of Kb into one another

A

b hydroxybutyrate can be converted to acetoacetate via enzyme b hydroxybutyrate, reaction is reversible and is dependant on level of Nad/Nadh

54
Q

ketogenissi

A
  1. mitochondria in liver
    substrate: acetyl co-a and acetoacetyl coa (which came from b oxidation) think of it as a step by step

2 key enzymes

  1. HMG COA synthase
  2. HMG COA lyase

acetoacetyl COA+acetyl COA= HMG COA

HMG CO A—acetoacetate+ acetyl COA

the acetoacetate can then be converted to any of the other 2 KB

55
Q

regulation of ketogenisis

A
  1. lipolysis-kb formation is enhanced when there is an increase of FFA in the blood that has cam from the breakdown of TAGS
56
Q

list the compariosn table betwen Kb and normal conditions

A

Normal:

ration of insulin /glucagon is low
leval of FFA in blood is low (because no lipolysis ha

57
Q

regulation of ketogenisis

A
  1. lipolysis-kb formation is enhanced when there is an increase of FFA in the blood that has cam from the breakdown of TAGS

Insulin and glucagon are key regulating hormones of ketogenesis. Both hormones regulate hormone-sensitive lipase and acetyl-CoA carboxylase. Hormone-sensitive lipase produces diglycerides from triglycerides, freeing a fatty acid molecule for oxidation. Acetyl-CoA carboxylase catalyzes the production of malonyl-CoA from acetyl-CoA. Malonyl-CoA reduces the activity of carnitine palmitoyltransferase I, an enzyme that brings fatty acids into the mitochondria for β-oxidation. Insulin inhibits hormone-sensitive lipase and activates acetyl-CoA carboxylase, thereby reducing the amount of starting materials for fatty acid oxidation and inhibiting their capacity to enter the mitochondria. Glucagon activates hormone-sensitive lipase and inhibits acetyl-CoA carboxylase, thereby stimulating ketone body production, and making passage into the mitochondria for β-oxidation easier

58
Q

list the comparison table between Kb and normal conditions

A

Normal:

ration of insulin /glucagon is low
level of FFA in blood is low (because no lipolysis happening)

insulin isi Inhibiting HSL ( in oH)

starvation/diabetes

ratio is high
a lot of FFA in blood
glucagon activating HSL (O-P)

59
Q

HSL regulation

A

active - phosphoralted

inactive _dephosphorolated

60
Q

terms related to kB

A

ketosis

normal process of the body -low levels of KB

Ketoacidosis
-abnormally high levels
can turn the blood acidic
occurs in diabetics who dont take enough insuline or alcohols or stravation

increased levels in blood-ketoanemia
increased in urine- ketourea
ketoacidosis: blood turning acidic

61
Q

characteristics of pUFA

A

cis isomers

have a pi bond due to p electrons

62
Q

biological function

A
  1. part of the phospholipids and glycoplipids what constitute cell membranes
  2. cell signalling
63
Q

biological function

A
  1. part of the phospholipids and glycoplipids what constitute cell membranes
  2. cell signalling
  3. substrate for the synthesis of eicosanoids
64
Q

essential PUFA

A

Linoleic acid and alpha linoleic acid. 18 C- (sesame sunflower) spinach (alpha)

Arachidonic acid (beef chicken pork) - is a weird one because it can be synthesised by us.

EPA+ DHA (same as arachidonic acid) eggs and fish

65
Q

guidlines for pUFA

A

recommend 2wice a week- fish diet

deficiency - dry and brittle hair, impaired growth, impaired reproductive functions , premature births

66
Q

omega 3 FA

A
  • improves blood circulaton-decreases viscoisty
  • anti aggregation effect (antithrombogenic)-decreases platelet aggregation
  • antiathreogenic -reduces LDL
  • antiinflammatory effect - because synthesis of antinflammatory eicosanoids

Protective effect on endothelium, making wall more flexible
lipotropic effect - protects the liver from fatty infiltration and accumulation of TAG

They are used in diseases such as
joint diseases - e.g lupus
hypertension
MI

67
Q

how does the body make PUFA

A

the first double bond is introduced in the delta 9 position by delta 9 destaturase. always in cis confrimation Need cytochrome b5/b5 reductase, happens in ER need reducing equivalents (either)

68
Q

examples of omega 3

A

DHA AND EPA

69
Q

eicosanoid pathway

A
  1. cylooxygenase pathway- prostanoids-prostaglandins and thromboanes
  2. lipoxygenase pathway-leukotrienes + lipoxins
70
Q

COX 1 AND COX 2

A

COX 1 -constituitive
COX 2 - inducible

inhibited by NSAIDS and aspirin

71
Q

biological leukotrienes

A

formed by . lipoxygenase pathway, leukotrienes are produced by white blood cells by the oxidation of arachidonic acid by arachidonate 5 lipoxygenase .

main function: reaisation of an immune response

LTB4- stimulate vessel permeability
LTC4, LTD4,LTE4 hypersentitvity/nphylatic reactions

72
Q

biological function of prostanoids

A

mediate inflammation, reproductios, blood clotting, blood pressure

made in low concentrations
have paracrine and autocrine effect
associated with G proteins

tissue hormones (not associated with glands)

73
Q

types of eicosanoids

A

type 2 : 6immune activators- stimulate platelet aggregation

type 3:3 immune supressors, inhibit platelet aggregartion

74
Q

where does ketolysis occur

A

mitochondria but not in the LIVER

75
Q

ketolyis AND STEPS

A

the process by which the kB produced by the liver and converted in extarhepatic tissues in order to produce acetyl COA

3 hydroxybutyrate is oxidised to acetoactic acid produce NADH —-ETC — ATP.
The ac-ac is gets converted into acetoacetyl coa by enzyme thiophorase using succinly coa as a donor.

then ac-ac is cleaved by thiolase to 2 acetyl coa for more krebs

76
Q

Which tissues use KB

A

brain, muscle, heart, nervous system

77
Q

conditions for TAG synthesis

A
  • activated glycerol

- activated fatty acids

78
Q

how are the fatty acids activated in order to make TAG

A

FA are activated with coenzyme A by the enzyme AYCYL COA synthetase (ATP)

79
Q

VLDL

A

main carrier of TAG, takes tag to adipocytes for storage the Tag are released by lipoprotein lipase which is found in the walls of blood vessels.

80
Q

main carriers of TAG

A

CM + VLDL

81
Q

2 forms of CM

A

nascent CM

mature after it exchanged proteins with HDL C2 + E

82
Q

LPL

A

breaks down CM to relase TAG in tissues needs to be activated by C2

83
Q

what causes the breakdown of TAG

A

HSL, due to glucagon activating via camp

active in its OP form

84
Q

glycerol kinase

A

found only in the liver
however in adipose there is no enzyme so we start of with DHAP (glycolsis) and convert it back to glycreol 3 phosphate via the enzyme glycerol 3 ph DH

85
Q

Glycerol metabolism

A
  1. glycolysis
  2. gluconeogensis
  3. resterifcation
86
Q

job of CM

A

deliver chol to liver

deliver TAG to tissues

cholesterol (2 decks)

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