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POM > Cholesterol > Flashcards

Cholesterol Flashcards

1
Q

What three primary are fats derived from?

A

The diet

De novo biosynthesis - liver

Storage depots in adipose tissue

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2
Q

Where are bile salts generated and stored? What do they do?

A

Generated by liver and stored in gallbladder

During digestion they pass from the bile duct into the intestine
Emulsify fats in the intestine aiding their digestion and absorption of fats and also that of fat-soluble vitamins A, D, E and K

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3
Q

What does a lack of bile salts lead to?

A

Majority of fat passes through the gut undigested and unabsorbed

This leads to steatorrhoea

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4
Q

What is orlistat/tetrahydrolipstatin?

A

Inhibitor of gastric and pancreatic lipases

chemically synthesised derivative of lipstatin (product of streptomyces toxytricini)

Reduces fat absorption by 30% which is then excreted faecally

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5
Q

Name the five lipoproteins and their sources

A

Chylomicrons - intestines

VLDLs - liver

IDL - VLDL

LDL - IDL

HDL - liver

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6
Q

Role of chylomicron?

A

Dietary fat transport

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7
Q

Role of VLDL?

A

Endogenous fat transport

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8
Q

Role of IDLs and LDLs?

A

IDLs - intermediate LDL precursor

LDL- cholesteron transport

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9
Q

Role of HDLs?

A

Reverse cholesterol transport

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10
Q

What do chylomicrons acquire from HDLs when released into the blood stream?

A

Apoproteins

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11
Q

Where do chylomicrons travel from and to, to get to the bloodstream?

A

From the lacteals of intestine to the thoracic duct and left subclavian vein where they enter the blood stream

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12
Q

Where is lipoprotein lipase found and what does it bind to?

A

Located on the capillary endothelial cells lining adipose tissue heart and skeletal muscle

Bind to apoproteins cleaving the chylomicron

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13
Q

What are the properties of the shell and core of a chylomicron?

A

Hydrophillic outer shell

Hydrophobic core

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14
Q

What is cholesterol and what does it do?

A

Cholesterol is a steroid

It increases or decreases membrane stiffness, depending on temperature and nature of membrane

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15
Q

Where is most of the cholesterol in our body found?

A

More than 90% in cell membranes

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16
Q

What is dietary uptake of cholesterol?

How are physiological requirements for cholesterol met?

A

0.5g/day

Supplied by the liver by de novo synthesis of cholesterol from acetyl-CoA

17
Q

What are the three main parts of the cholesterol synthesis pathway and where do they occur?

A
  • synthesis of isopentenyl pyrophosphate, activated isoprene unit - key building block (cytoplasm)
  • Condensation of six molecules of isopentenyl pyrophosphate to form squalene (cytoplasm)
  • cyclisation and demethylation of squalene by monooxygenase to give cholesterol (ER)
18
Q

What are four steps of isopentenyl pyrophosphate synthesis?

A
  1. Condensation of 2 Acetyl-CoA molecules to form acetoacetyl CoA using β=ketothiolase
  2. further condensation by acetyl-CoA via HMG-CoA synthase to form HMG-CoA
  3. HMG-CoA reduced to form mevalonate via HMG-`CoA reductase
  4. Mevalonate sequentially phosphorylated at hydroxyl groups positions, then decarboxylated to form 3-isopentenyl pyrophosphate
    enzymes: mevalonate kinase, phosphomevalonate kinase, kinase, phospho mevalonate decarboxylase
19
Q

What is HMG-CoA reductase under negative feedback control by?

A

End product cholesterol, bile salts and the mevalonate intermediate

20
Q

What does the isoprene unit do?

A

Confers lipophilicty to biomolecules - gives them affinity for lipid bilayers

21
Q

What two steps produce squalene from the isoprene unit?

A
  1. Dimethylallyl pyrophosphate can be produced from isopentyl pyrophosphate via isopentenyl isomerase

This then condenses with a unit of isopentenyl-pp to form Geranyl pyrophosphate (C10 compound)

Third isopentenyl-PP molecule is added to form fernesyl pyrophosphate (C15 intermediate)

  1. Two farnesyl pyrophospate molcules condense via squalene synthase to form C30 squalene and two molecules of pyrophosphate
22
Q

What are the three steps in which squalene is cyclised to cholesterol?

A

1, squalene is reduced in the presence of O2 and NADPH to form squalene epoxide via squalene epoxidase

  1. enzyme squalene epoxide lanosterol-cyclase catalyses formation of lanosterol - formation of four rings occurs
23
Q

What are the three steps in which squalene is cyclised to cholesterol?

A

1, squalene is reduced in the presence of O2 and NADPH to form squalene epoxide via squalene epoxidase

  1. enzyme squalene epoxide lanosterol-cyclase catalyses formation of lanosterol - formation of four rings occurs
  2. Lanosterol is subsequently reduced and demethylated to generate cholesterol
24
Q

How is pregnenolone generated from cholesterol?

A

By the action of the enzyme desmolase

25
Q

What are the 5 classes of steroid hormones from pregnenalone?

A

Progestogens

Glucocorticoids

Mineral corticoids

Androgens

Estrogens

26
Q

What are bile salts?

A

Major breakdown products of cholesterol and account for half of the 800mg of cholesterol made each day

27
Q

Explain the anatomy of a lipoprotein?

A

phospholipid monolayer containing cholesyerol and apoproteins

Surrounds a core of cholesterol esters and triacylglycerols

28
Q

How are cholesterol esters formed?

A

Synthesised in plasma from cholesterol and the acyl chain of phospahtidylcholine (lecithin) via lecithin:cholesterol acyltransferase (LCAT)

29
Q

What is good cholesterol and why?

A

HDL - take cholesterol from peripheral tissues back to the liver for use or disposal (reverse cholesterol transport) -
lower total serum cholesterol

30
Q

Whats bad cholesterol and why?

A

LDLs - prolonged elevation leaads to astherclerosis

Transport cholesterol synthesisded in liver to peripheral tissues with more than 40% of their weight made up of cholesterol esters

31
Q

What is familial hypercholesterolaemia?

A

Monogenic dominant trait

Cholesterol transportation is defective and cholesterol level is 2-3 times higher

Susceptible to atherosclerosis in middle age

32
Q

What is the general mechanism behind familial hypercholesterolaemia?

A

LDLs give rise to a form of cholesterol called LDL-derived cholesterol

This form is usually taken up by LDL receptors (LDLR)

Patients with severe FH lacked functional LDLRs along their fibroblasts

So they are unable to take up the the LDL-derived cholesterol

33
Q

What are the two ways to control hypercholesterolaemia?

A

Resins/sequestrants - such as cholestyramine bind to sequester bile acid-cholesterol complexes preventing their reabsorption by the intestine and can lower LDL by 15-30% and raise HDL by 3-5%

HMG-CoA reductase inhibitors- competitive inhibitor of HMG-CoA Reductase aka statins e.g. - Lovastatin, lipitor
This prevents formation of mevalonate in step 3 of cholesterol biosynthesis

33
Q

What are the two ways to control hypercholesterolaemia?

A

Resins/sequestrants - such as cholestyramine bind to sequester bile acid-cholesterol complexes preventing their reabsorption by the intestine and can lower LDL by 15-30% and raise HDL by 3-5%

HMG-CoA reductase inhibitors- competitive inhibitor of HMG-CoA Reductase aka statins e.g. - Lovastatin, lipitor
This prevents formation of mevalonate in step 3 of cholesterol biosynthesis

34
Q

What are the two ways to control hypercholesterolaemia?

A

Resins/sequestrants - such as cholestyramine bind to sequester bile acid-cholesterol complexes preventing their reabsorption by the intestine and can lower LDL by 15-30% and raise HDL by 3-5%

HMG-CoA reductase inhibitors- competitive inhibitor of HMG-CoA Reductase aka statins e.g. - Lovastatin, lipitor
This prevents formation of mevalonate in step 3 of cholesterol biosynthesis

35
Q

Explain the process of receptor mediated endocytosis of LDL

A

LDL binds to LDL receptors
Endocytosis of clathrin coated vesicle
Uncoating
Fusion with endosome
TRansfer to lysosome > free cholesterol released
Budding off of transport vesciles
return of LDL receptors to plasma membrane

36
Q

Explain the process of receptor mediated endocytosis of LDL

A

LDL binds to LDL receptors
Endocytosis of clathrin coated vesicle
Uncoating
Fusion with endosome
TRansfer to lysosome > free cholesterol released
Budding off of transport vesciles
return of LDL receptors to plasma membrane

POM (42 decks)

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