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POM > Molecular Biology - Cholestrol > Flashcards

Molecular Biology - Cholestrol Flashcards

1
Q

3 main sources fats are derived from

A

Diet
De novo biosynthesis in the liver
Storage deposits in adipose

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2
Q

What are deitary fats broken down by?

A

Lipases

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3
Q

Where are bile salts generated and stored?

A

Liver and gallbladder respectively

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4
Q

Bile salts during digestion?

A

Pass from bile duct into intestine where they emulsify fats in the intestine, aiding their digestion and absorption of fats + fat-soluble vitamins

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5
Q

Lack of bile salts

A

Majority of fat passes through undigested resulting in steatorrhea (fatty stool)

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6
Q

Treatment for obesity

A

Orlistat is a gastric/pancreatic lipase inhibitor and derivative of lipstatin so reduces fat absorption

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7
Q

What type of lipoprotein has a role in dietary fat transport?

A

Chylomicrons - source is in the intestine

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8
Q

Anatomy of chylomicron?

A

Single phospholipid bilayer with apoproteins on outside and triglycerides in the middle

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9
Q

How is chylomicron created?

A

Digested dietary products are absorbed by enterocyte that line brush border ; triglycerides are resynthesized and transported via lymphatics

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10
Q

When do chylomicrons aquire apoproteins?

A

From HDL following release into bloodstream

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11
Q

Mechanism of action of chylomicron on heart/adipose/skeletal?

A

Binds to lipoprotein lipase and the fatty acids undergo beta oxidation while glycerol is returned to liver for gluconeogenesis

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12
Q

Special about chylomicrons?

A

Hydrophilic outside
Hydrophobic core

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13
Q

What type of molecule is cholestrol

A

Steroid

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14
Q

Cholestrol uptake/amount needed?

A

All physiological requirements for cholestrol are supplied by liver through de novo synthesis of cholestrol from acetyl-coA

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15
Q

Cholestrol synthesis

A

1 pathway 3 parts
1) Cytoplasm - isopentyl pyrophosphate synthesis
2) Cytoplasm - 6 molecules of step 1 condensation to form squalene
3) ER - cyclisation/demethylation of squalene gives cholestrol

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16
Q

Step 1 of step 1

A

Needs two Acetyl CoA molecules condensation and releases coA

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17
Q

Main step of step 1

A

When creating mevalonate ; HMG-CoA reductase is negative feedback loop by end product cholestrol and mevalonate/bile salts

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18
Q

What happens in main step?

A

NADPH is oxidised to NADP and coA is removed
(redox)

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19
Q

To finish off step 1?

A

Sequential phosphorylation and decarboxylation

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20
Q

Second step?

A

3 condensation reactions of 5 carbon unit structures to make a C15 molecule ; two of which condense to form squalene

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21
Q

Step 3

A

Cyclisation + demethylation

22
Q

how is cholestrol basis of all steroid hormones?

A

It producs the precursor called pregnenolone by enzyme desmolase

23
Q

5 classes of steroid hormones?

A

Glucocorticoids
mineralocorticoids
androgens
estrogens
progestagens

24
Q

What can vitamin D deficiency lead to?

A

Rickets

25
Q

Synthesis of vitamin D

A

Exposure of skin to sunlight

26
Q

Cholestrol and bile salts?

A

bile salts are major breakdown products of cholestrol ; glycholate and taurocholate

27
Q

Source and role of VLDL

A

Liver ; endogenous fat transport

28
Q

Source and role of IDL

A

VLDL and precursor to LDL

29
Q

Source and role of LDL

A

IDL - cholestrol transport

30
Q

Source and role of HDL

A

Liver - reverse cholestrol transport

31
Q

Lipoprotein

A

Cholestrol esters and triacylglycerols in middle with single phospholipid bilayer outside containing apoproteins and cholestrol

32
Q

Cholestrol to cholestrol ester

A

Synthesized in PLASMA from cholestrol and lecithin ; via catalyses of LCAT

33
Q

VLDL synthesis

A

In liver and then released into circulation

34
Q

HDLs synthesis

A

In liver and smal intestine and take up lipids/cholestrol from tissue back to the liver

35
Q

IDLs syntehsis

A

Triacylglycerol removal from VLDL

36
Q

LDLs synthesis

A

Cholestrol ester transfer from HDL to IDL

37
Q

Bad vs good cholestrol

A

HDL = good cholestrol ; take cholestrol from peripheral tissue back to the liver for use/disposal and lower cholestrol levels
LDL = leads to atherosclerosis if prolonged elevation - transport cholestrol from liver to periphery

38
Q

Bile acids?

A

Cycle between intestine and liver

39
Q

Chylomicrons cycle?

A

Free fatty acids are released (to build up adipose tissue etc) and remnants are left over to then return to the liver

40
Q

Familial hypercholestrolaemia

A

Monogenic dominant trait - they have serum that is 2/3 times the normal level and are susceptible to atherosclerosis (single copy of gene)

41
Q

Those with both copies of mutant gene for FH

A

Severely affected 5* as much cholestrol and coronary infarcts/atherosclerosis in adolescence

42
Q

Homozygous FH

A

Two faulty copies of mutant gene

43
Q

Symptoms of FH

A

Xanthomas lying superficially ; deposition of LDL-derived cholestrol

44
Q

Fibroblast

A

Contributes to formation of connective tissue

45
Q

In FH what happens to the fibroblasts

A

THEY LACK LDL RECEPTORS SO UNABLE to take up cholestrol

46
Q

LDL endocytosis?

A

Endocytosis
Uncoating
Fusion with endoscope (and subsequent lysosome breakdown)
Budding off vesicles
Return of LDL receptors to membrane

47
Q

How to control FH using statins?

A

Statins like lipitor has similar structure as mevalonate so end product inhibition of HMG-CoA reductive preventing synthesis of cholestrol

48
Q

Mode of action of Resins?

A

Bind to bile acid-cholestrol complexes preventing reabsorption by the intestine

49
Q
A
50
Q
A

POM (12 decks)

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