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103 Theme 3 - Cardiovascular System > Lipid metabolism and pathways > Flashcards

Lipid metabolism and pathways Flashcards

1
Q

What are the biological functions of lipids?

A
  • Essential components of cell membranes e.g. phospholipids, glycolipids, cholesterol
  • Inter- and intra-cellular signalling events e.g. precursor of steroid hormones
  • Energy generation and fuel storage i.e. triglycerides
  • Metabolism e.g. bile acids
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2
Q

What type of lipid are storage lipids made of?

A

Triacylglycerols

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3
Q

What are triacylglycerols also known as?

A

fats or triglycerides (TG)

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4
Q

What form of lipids constitutes 90% of dietary lipids?

A

Triacylglycerols

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5
Q

What is the role of triacylglycerols?

A

Major form of metabolic energy storage in humans

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6
Q

Are triacylglycerols hydrophillic or hydrophobic?

A

Hydrophobic

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7
Q

Draw the basic composition of a triacylglyercol

A
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8
Q

What does unsaturated mean?

A

‘unsaturated’ means the presence of double bonds between two carbon atoms

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9
Q

What are the 2 major metabololic pathways for the metabolism of triacylglycerides?

A

TGs broken into free fatty acids and glycerol. Oxidation of fatty acids in the mitochondria to release energy in the form of ATP.

Synthesis of fatty acids from acetyl-CoA (joined to a glycerol molecule for storage).

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10
Q

What are the 3 stages to achieve complete oxidation of fatty acids to CO2 and H2O?

A
  1. Removal of glycerol and oxidation of long chain fatty acids to 2-carbon fragments in the form of acetyl-CoA: THIS IS β-OXIDATION
  2. Oxidation of acetyl-CoA to CO2 in the citric acid cycle
  3. Transfer of electrons from reduced electron carriers to mitochondrial respiratory chain
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11
Q

What are the 3 steps in beta oxidation of fatty acids?

A

1st step: fatty acids activated by attachment to Coenzyme A (CYTOSOL)

2nd step: transfer of acyl-groups across mitochondrial membrane (RATE-LIMITING STEP)

3rd step: progressive oxidation of fatty acids by removal of 2-carbon units to form acetyl-CoA which enters the citric acid cycle

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12
Q

Where does β-oxidation of fatty acids occur?

A

β-oxidation of fatty acids occurs in mitochondria, also in peroxisomes

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13
Q

How does attatchement to Co-A happen in beta oxidation of fatty acids?

A
  1. Carnitine transfers fatty acid across the membrane to matrix
  2. CoA isn’t transferred over; there is 2 pools of CoA, one in the cytosol and one in the matrix
  3. Once the acyl group is moved across to the matrix, it is once again joined to CoA
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14
Q

What enzymes regulate attachement to Co-A in beta oxidation of fatty acids?

A

This is regulated by the enzymes carnitine palmitoyl transferase I and II.

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15
Q

This diagram shows the 3rd step of beta oxidation of fatty acids.

What happens at each cycle in the diagram?

A

Each cycle: Shortens fatty acid by 2C

1 acetyl-CoA formed

1 FADH2 formed

1 NADH formed

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16
Q

What are the products of beta oxidation of fatty acids used for?

A

Used to generate energy for the cell

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17
Q

Which enzymes in beta oxidation of fatty acids cause SIDS when mutated?

A

Group of dehydrogenase isozymes

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18
Q

The whole beta oxidation process is repeated over and over again until when?

A

Whole process is repeated until completely broken into acetyl-CoA

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19
Q

Where does fatty acid synthesis occur?

A

Occurs mainly in liver and adipocytes

Occurs in the cytosol

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20
Q

How does fatty acid synthesis work?

A

Long carbon chain molecules built up from 2-carbon units derived from acetyl CoA

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21
Q

How does acetyl CoA get out of the mitochondria and into the cytosol for fatty acid synthesis to occur?

A

The citrate-malate cycle

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22
Q

Complete the diagram on the citrate malate cycle

A
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23
Q

What is the equation of fatty acid biosynthesis?

A

Citrate -> Acetyl CoA -> Malonyl CoA

24
Q

What is the rate limiting step in the fatty acid biosynthesis equation?

A
25
Q

What happens in fatty acid biosynthesis?

A
  • Malonyl CoA and acetyl CoA both bind to fatty acid synthase
  • A series of condensation reactions involving malonyl CoA adds further C2 units
26
Q

What are the rate limiting steps in fatty acid oxidation and synthesis?

A

Beta oxidation: transfer of acyl-CoA into mitochondria

Fatty acid synthesis: formation of malonyl CoA from acetyl-CoA, catalysed by acetyl CoA carboxylase

27
Q

What part of fatty acid oxidation and synthesis is subject to control by glucagon and insulin?

A

Formation of malonyl CoA from acetyl-CoA, catalysed by acetyl CoA carboxylase

28
Q

Why is cholesterol essential to life?

A

In healthy organism, balance maintained between biosynthesis, utilisation and transport – keeping harmful deposition to a minimum

29
Q

What does cholesterol deposition in arteries lead to?

A

Deposition in arteries associated with heart disease and stroke

30
Q

What are the 3 physiological roles of cholesterol?

A

a) Important lipid component of biological membranes
b) Precursor of steroid hormones
c) Source of bile acids

31
Q

What 3 things do bile acids aid in?

A

a) lipid digestion
b) lipid absorption
c) cholesterol excretion

32
Q

What are bile acids?

A

Bile acids are polar derivatives of cholesterol

33
Q

What is the biochemical structure of cholesterol?

A

Amphipathic lipid (hydrophobic and hydrophilic portions)

34
Q

What is cholesterol synthesised from and eliminated as?

A

Synthesized from acetyl CoA and eliminated as bile acids

35
Q

What is the storage form of cholesterol and where is it found?

A

Storage form is cholesterol ester found in most tissues

36
Q

What part of the cholesterol molecule makes it amphipathic?

A

The OH

37
Q

Which enzyme catalyses the formation of cholesterol esters?

A

Cholesterol Acyltransferases e.g. Acyl-CoA Cholesterol Acyltransferase (ACAT) catalyses formation of cholesterol esters

38
Q

Draw the structure of a cholesterol ester

A
39
Q

How many stages are there in cholesterol biosynthesis?

A

4

40
Q

Draw cholesterol biosynthesis

A
41
Q

Where does cholesterol biosynthesis occur?

A

Major site of synthesis is the liver; lesser amounts made in intestine & adrenal cortex

42
Q

Where is the rate determining step and name 2 inhibitors which work here

A
  • cholesterol is feedback inhibitor
  • mevalonate is feedback inhibitor

HMG-CoA Reductase activity also regulated by insulin/glucagon

43
Q

Where is the target site for statin drugs?

A
44
Q
A
45
Q

Why is transport of lipids round the body needed?

A
  • Bring dietary lipids to cells for energy production or storage
  • Move lipids from storage in adipose tissue for use in energy production
  • Provide lipids from the diet to cells for synthesizing cell membranes
  • Carry cholesterol from peripheral tissues to the liver for excretion
46
Q

What 2 ways are lipids transported in the blood?

A
  • Short-chain fatty acids are transported bound to blood proteins like albumin
  • Bulk transport of neutral lipids, which are insoluble in water, requires special carrier proteins: lipoproteins
47
Q

What is the structure of a lipoprotein?

A
  • Neutral lipids carried in a central core
  • Outer layer of amphipathic phospholipids and cholesterol
48
Q

What are the 4 types of lipoproteins?

A

VLDL – Very Low Density Lipoproteins

IDL – Intermediate Density Lipoproteins

LDL – Low Density Lipoproteins

HDL – High Density Lipoproteins

49
Q

What is the only lipoprotein that’s major apolipoprotein is not E?

A

LDL

B-100 apolipoprotein

50
Q

Put the lipoproteins in order of size from smallest to biggest

A

Diameters (nm)

Chylo, 50-200

VLDL, 28–70

LDL, 20-25

HDL, 8-11

51
Q

What is the role of each lipoprotein?

A

Chylomicrons: deliver dietary TGs to muscle and adipose tissue + dietary cholesterol to the liver

VLDL: transport endogenous TGs and cholesterol

LDL: transport cholesterol from liver to tissues

HDL: transport cholesterol from tissues to liver i.e. remove cholesterol from tissues

52
Q

What is the role of IDL?

A

IDL formed from lipid depleted VLDL

Allows release of TG at tissues

53
Q

How does lipid uptake by cells occur?

A
  • Chylomicrons and VLDL particles give up lipid (TG) to tissues by the action of tissue-bound lipases
  • The liver recognises remnants of these particles by their ApoE content, and takes them up for re-cycling
  • LDL particles contain ApoB-100, which is recognised by cell surface LDL receptors (LDLRs)
54
Q

What is the result of LDL (cholesterol) uptake by cells?

A

Uptake of cholesterol results in decrease in cholesterol

& LDLR synthesis

55
Q

What is PCSK9?

A

PCSK9 – proprotein convertase subtilisin/kexin type 9

PCSK9 binds to LDL receptor and results in it’s degradation

56
Q

What happens to LDLR when there’s low cholesterol?

A

Expression of LDL receptors increased by SREBPs in response to low cholesterol

SREBP exported to Golgi when cholesterol is low

Activation of SREBP increases HMGCR activity and expression of LDLR

103 Theme 3 - Cardiovascular System (19 decks)

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