Lipid metabolism Flashcards

(37 cards)

1
Q

What are the three classes of lipids

A
  • fatty acid derivative
  • hydroxy-methyl-glutaric acid
  • vitamins
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2
Q

what types of lipids are fatty acid derivatives

A
  • fatty acids
  • triacylglycerols
  • phospholipids
  • eicosanoids
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3
Q

what types of lipids are hydroxy-methyl-glutaric acids

A
  • ketone bodies
  • cholesterol
  • cholesterol esters
  • bile acids and salts
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4
Q

what type of vitamins are lipid soluble

A

A
D
E
K

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5
Q

what and where is the first stage of lipid metabolism

A

extracellular digestion in GI tract

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6
Q

how are triacylglycerols first metabolised in the GI tract

A
  • hydrolysed by pancreatic lipase in small intestine
    broken into glycerol and fatty acids
    (requires bile salts and protein factor colipase)
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7
Q

after triacylglycerols are broken into glycerol and fatty acids where does the glycerol go

A

enters blood to liver to be metabolised

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8
Q

how does the liver metabolise glycerol

A
  • phosphorylated by glycerol kinase to glycerol phosphate which can either be used for triacylglycerol synthesis or enter glycolysis by converting DHAP
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9
Q

How are triacylglycerols stored

A
  • converted to triacylglycerol in GI
  • packed into lipoprotein particle called chylomicrons
  • travel through lymphatics to adipose tissue where stored
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10
Q

What is lipolysis

A

the release of lipids from storage when needed
- hormone controlled
- stimulated by high adrenaline and glucagon
- inhibited by insulin

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11
Q

How are lipids released from lipolysis carries to tissues

A

by blood covalently bound to albumin= albumin-fatty acid complex

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12
Q

What are the three stages of fatty acid metabolism

A

1) activation
2) transport to mitochondria
3) b- oxidation

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13
Q

How are fatty acids activated for metabolism

A

by linking to CoA via S atom forming high energy hydrolysis bond
via enzyme: fatty acyl CoA synthase

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14
Q

How are fatty acids transported to the mitochondria

A

via carnitine shuttle

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15
Q

Why do fatty acids require a carnitine shuttle for transport to mitochondria

A

activated fatty acids do not readily cross inner membrane of mitochondria

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16
Q

Describe the action of the carnitine shuttle

A
  • acyl group transferred to carnitine by CAT1 (carnitine acyltransferases 1) which then moves across the mem
  • acyl group from acyl carnitine transferred to CoA on inside using CAT2
17
Q

how is the transport of fatty acids to mitochondria regulated

A
  • AMP and insulin
    -inhibited by malonyl CoA (intermediate of FA synthesis) as means new FA made do not go directly to mitochondria
18
Q

Describe the process of beta oxidation

A
  • a spiral that removes a C2 unit (acetate) each time until only 2C remain which are all bound to CoA to make acetyl CoA
19
Q

What molecules does beta oxidation require

20
Q

What are the features of triacylglycerols

A
  • hydrophobic
  • stored in anhydrous form (no water weight)
  • stored in adipose tissue
  • used in exercise, starvation and pregnancy
21
Q

What are the three ketone bodies produced in the body

A

-acetoacetate
- acetone
- B- hydroxybutyrate

22
Q

what are features of ketone bodies

A
  • soluble in water
  • produced when acetyl CoA is high
  • used by muscle
  • alternative fuel to glucose in brain as can cross blood brain barrier
23
Q

Where are ketone bodies synthesised

24
Q

What does the first enzyme do in ketone body synthesis do

A

Enzyme : synthase
function: converts acetyl CoA to Hydroxymethyl glutaryl-CoA (HMG-CoA)

25
What can HMG-CoA be converted
- to ketone bodies by enzyme lyase HMG-CoA --> acetoacetate which can either degrade into acetone or be converted to beta-hydroxybutyrate - to cholesterol via enzyme HMG - CoA reductase
26
What enzyme do statin drugs target
HMG - CoA reductase
27
how is synthesis of ketone bodies controlled
controlled by inhibition of TCA cycle so acetyl CoA diverted to ketone synthesis - low NAD or high NADH enzymes of TCA cycle inhibited so acetyl CoA diverted
28
How are ketone bodies synthesised
acetoacetate enters blood and is converted to acetoacetyl in muscle as is a intermediate of TCA
29
how is ketone synthesis regulated in the fed state
- fed means high insulin so inhibits lyase and reductase activated so cholesterol synthesis
30
how is ketone synthesis regulated in the early starvation state
- starvation means low insulin and high glucagon - lyase activated and reducatase inhibited so ketone synthesis
31
how do ketone bodies spare glucose
reserve glucose for brain and other tissues use ketone bodies
32
how do ketone bodies spare glucose in late starvation
- very low insulin - ketones produced for all other tissues but glucose for brain from breakdown of muscle and glycogen
33
what happens in diabetes with ketone production and glucose
- high glucose as not being utlilised - ketone bodies still being produced as glucose not used so uncontrolled ketogenesis
34
what are the plasma levels of ketones in the normal state
less than 1nm
35
what are the plasma levels of ketones in the starvation state
2-5nm (physiological ketosis)
36
what are the plasma levels of ketones in diabetes
greater than 10m (pathological ketosis)
37