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ChemPath > Lipid metabolism > Flashcards

Lipid metabolism Flashcards

1
Q
  1. What are the features of an atherosclerotic lesion?
A 
Fibrous cap 
Foam cells (macrophages full of cholesteryl ester) 
Necrotic core (full of cholesterol crystals)
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2
Q
  1. What is the biggest plasma lipoprotein?
A

Chylomicrons

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3
Q
  1. During what time will chylomicrons be most abundant?
A

After eating (they are present in very small amounts in the fasted state)

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4
Q
  1. Describe the uptake of cholesterol by the intestinal epithelium.
A

Cholesterol entering the intestines will come from the diet and bile
Cholesterol will be solubilised in mixed micelles
It is then transported across the intestinal epithelium by NPC1L1 (this is the main determinant of cholesterol transport

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5
Q
  1. Name two transporters that transport cholesterol back into the intestinal lumen.
A

ABC G5

ABC G8

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6
Q
  1. Where are bile acids absorbed?
A

Terminal ileum

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7
Q
  1. What happens when cholesterol arrives at the liver?
A

Downregulates the activity of HMG CoA reductase

NOTE: this is responsible for the production of cholesterol from acetate and mevalonic acid

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8
Q
  1. What are the two fates of cholesterol that is either produced by or transported to the liver?
A

Hydroxylation by 7alpha-hydroxylase to produce bile acids

Esterification by ACAT to produce cholesterol ester which is incorporated into VLDLs along with triglycerides and ApoB

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9
Q
  1. Which transfer protein is important in the packaging of VLDLs?
A

MTP

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10
Q
  1. Which transfer protein is important in the packaging of HDLs?
A

ABC A1

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11
Q
  1. What are the effects of CETP on the movement of substances between lipoproteins?
A

Moves cholesterol from HDL - VLDL

Moves triglycerides from VLDL - HDL

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12
Q
  1. Which receptor is responsible for the uptake of some HDLs by the liver?
A

SR B1

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13
Q
  1. Describe the transport and metabolism of triglycerides.
A

Triglycerides from fatty foods are hydrolysed to fatty acids, absorbed, and resynthesized into triglycerides which are transported by chylomicrons into the plasma
Chylomicrons are hydrolysed by lipoprotein lipase into free fatty acids
Some free fatty acids are taken up by the liver, and some by adipose tissue
The liver resynthesizes fatty acids into triglycerides and packages them into VLDLs
VLDLs are acted upon by lipoprotein lipase to liberate free fatty acids

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14
Q
  1. List the three causes of familial hypercholesterolaemia (type II).
A

Caused by autosomal dominant gene mutations in:
LDL receptor
ApoB
PCSK9

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15
Q
  1. List some mutations that are implicated in polygenic hypercholesterolaemia.
A

NPC1L1
HMGCR
CYP7A1

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16
Q
  1. What is familial hyperalphalipoproteinaemia?
A

Increase in HDL caused by deficiency of CETP

This is associated with longevity

17
Q
  1. Describe the function of the LDL receptor.
A

LDLs bind to LDLR in coated pits which then undergo endocytosis (thereby uptaking the LDL into the liver)

18
Q
  1. List some clinical features of familial hypercholesterolaemia.
A

Xanthelasma
Corneal arcus
Tendon xanthomata

19
Q
  1. What is PCSK9?
A

A protein that binds to LDL receptors and degrades them

NOTE: gain of function mutations result in increased breakdown of LDLR and hence increased plasma LDL levels

20
Q
  1. List the key features of the following forms of familial hypertriglyceridaemia:

Familial type I
Type VI
Type V

A

a. Familial Type I
Caused by deficiency of lipoprotein lipase and ApoC II
NOTE: lipoprotein lipase degrades chylomicrons and ApoC II is an activator of lipoprotein lipase
b. Familial Type IV
Characterised by increased synthesis of triglycerides
c. Familial Type V
Characterised by deficiency of ApoA V
NOTE: these hypertriglyceridaemias show different patterns when the plasma is left overnight to separate

21
Q
  1. What is familial combined hyperlipidaemia?
A

Some people in the family have high cholesterol and others have high triglycerides

22
Q
  1. What is familial dysbetalipoproteinaemia (type III)?
A

Due to aberrant form of ApoE (E2/2)
NOTE: normal form is ApoE (3/3)
A diagnostic clinical feature of yellowing of the palmar crease (palmar striae)

23
Q
  1. List some causes of secondary hyperlipidaemia.
A

Pregnancy
Hypothyroidism
Obesity
Nephrotic syndrome

24
Q
  1. List four causes of hypolipidaemia and their underlying genetic defect.
A 
A-lipoproteinaemia
•	Autosomal recessive 
•	Extremely low levels of cholesterol 
•	Due to deficiency of MTP 
Hypo-lipoproteinaemia
•	Autosomal dominant 
•	Low LDL
•	Caused by mutations in ApoB 
Tangier disease
•	Low HDL
•	Caused by mutation of ABC A1 
Hypo-lipoproteinaemia
•	Sometimes caused by mutation of ApoA1
25
Q
  1. Describe the role of LDL in atherosclerosis.
A

LDL becomes oxidised once it has got through the vascular endothelium
Once oxidised it is taken up by macrophages
Within the macrophages, the LDLs become esterified and you develop foam cells

26
Q
  1. List some lipid-lowering drugs and their effect on lipid levels.
A

Statins – reduce LDLs, increase HDLs, slight increase in triglycerides
Fibrates – lower triglycerides, little effects on LDL/HDL
Ezetimibe – reduces cholesterol absorption (blocks NPC1L1)
Colestyramine – resin that binds to bile acids and reduces their absorption

27
Q
  1. List some novel forms of lipid-lowering drugs.
A

Lomitapide – MTP blocker
REGN727 – anti-PCSK9 monoclonal antibody
Mipomersen – anti-sense ApoB oligonucleotide

28
Q
  1. List three types of bariatric surgery.
A

Gastric banding
Roux-en-Y gastric bypass
Biliopancreatic diversion

29
Q
  1. List some beneficial effects of bariatric surgery.
A 
Reduced diabetes risk 
Reduced serum triglycerides 
Increased HDLs 
Reduced fatty liver 
Reduced blood pressure

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