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Medical Cell Biology and Genetics > L10- Lipid metabolism > Flashcards

L10- Lipid metabolism Flashcards

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1
Q

lipids are

A

insoluble- hydrophobic

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2
Q

lipids most commonly contain

A

C, H and O

-

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3
Q

phospholipids also contain

A

P and N

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4
Q

lipids are more …. than carbohydrates

A

reduced

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5
Q

what does it mean if lipids are more reduced than CHOs

A

release more energy when oxidised (requires more oxygen too)

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6
Q

classes of lipids

A
  1. Fatty acid derivatives
  2. Hydroxy-methyl-glutaric acid derivative (C6 compounds)
  3. Vitamins
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7
Q

Fatty acid derivatives

A
  • Fatty acids- fuel molecules
  • Triglycerides (TAG)- fuel storage and insulation
  • Phospholipids- membranes
  • Eicosanoids
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8
Q

Hydroxy-methyl-glutaric acid derivative (C6 compounds)

A
  • Ketone bodies- water soluble fuel molecules
  • Cholesterol- membrane and steroid hormones
  • Cholesterol esters
  • Bile acids and salts
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9
Q

vitamins

A

A, D, E, K

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10
Q

Triglycerides (TAG) structure

A
  • Glycerol backbone
  • Fatty acid side chain
  • Hydrophobic
  • Amphiphatic
  • Formed via esterification
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11
Q

TAG stored in

A

anhydrous form in adipose tissue

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12
Q

when is TAG utilised

A

prolonged exercise, starvation and during pregnancy

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13
Q

TAG gets hydrolysed to

A

glycerol and fatty acids

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14
Q

fatty acids produce how much of the energy of TAG

A

95% (B-oxidation)

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15
Q

glycerol produces how much of the energy of TAG

A

5% ( glycolysis)

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16
Q

TAG cannot be used by

A

cells without mitochondria

e.g. RBC and the brain (FA cannot pass BBB)

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17
Q

outline how triglycerides (TAG) is metabolised

A
  1. Triglycerides (TAG/ dietary lipids) eaten
  2. In the GI tract (small intestine) TAG is hydrolysed by pancreatic lipases
  3. TAG  Glycerol + fatty acids
    o Glycerol
  4. Glycerol is absorbed into the blood from the small intestine
  5. Glycerol in the blood is transported to the liver
  6. Where it is used as a precursor to synthesise glucose
    o Fatty acids
  7. FAs absorbed into the blood from the small intestine after TAG is broken down
  8. In the GI tract fatty acids are converted back to TAG
  9. In the blood TAG is then transported to the adipose tissue by lipoprotein particles called Chylomicrons
  10. Stored as TAG in adipose tissue
  11. Released as fatty acids when needed and carried to consumer tissues as albumin-fatty acid complex
  12. FA oxidation leads to release of ATP (energy)
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18
Q

structure of fatty acid

A

CH3(CH2)nCOOH

  • sat or unsatisfyingly
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19
Q

unsat

A

at least one double carbon bond)

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20
Q

name a FA is an essential requirement for the diet

A

linolenic acid

21
Q

FA metabolism simple: consumer tissue vs adipose tissue

A
  • Consumer tissue = FA oxidation –>energy
  • Adipose tissue (Stored as TAG) –> Fat mobilisation-hormone sensitive lipase
    o Increase- glucagon/adrenaline
    o Decrease- Insulin
22
Q

when is TAG mobilised from adipose tissue

A

glucagon or adrenaline

23
Q

fatty acid metabolism summary

A

Where? The mitochondria

  1. FA is activated by linking Coenzyme A outside the mitochondrion
  2. FA is transported across the inner mitochondrion using a carnitine shuttle
  3. FA cycles through sequence of oxidative reactions, with 2 Carbons removed each cycle- B-oxidation
24
Q

we want to oxides the fatty acid to

A

extract as many electrons as possible so that they can be transferred to electron carrying molecules like NAD+ and FAD+, so that NADH and FADH2 can be used to produce ATP on the electron transport chain.

25
Q

fatty acid activation

A

Fatty acyl CoA synthase links Coenzyme A to fatty acid

26
Q

activated fatty acids (Acyl-CoA)

A

do not readily cross the inner mitochondrial membrane

27
Q

what is coenzyme A derived from

A

vitamin B5

28
Q

outline the carnitine shuttle of fatty acyl-CoA

A
  • Fatty acyl-CoA (activated fatty acid) binds to carnitine to produce Acyl Carnitine (losing CoA)
  • Acyl carnitine is then transported across the mitochondrial membrane via the Carnitine shuttle transporter
  • Once within the Acyl Carnitine loses carnitine and recombines with CoA to form Acyl-CoA
29
Q

what inhibits carnitine shuttle

A

malonyl-CopA

30
Q

B-oxidation of Acyl-CoA

A

Where activated fatty acid chain get oxidised within B-oxidation cycle, which breaks the off 2 carbon chains per round- H+ and e- transferred to NADH and FADH2 (oxidation in ETC)

31
Q

2 carbon chains produced via B-oxidation are caleld

A

Acetyl Co-A

32
Q

Acetyl CoA prodded from B-oxidation

A

enter Kreb cycle and then the ETC to produce ATP

33
Q

glycerol is transported in the blood to the

A

liver where it is metabolised

34
Q

in the liver what starts the metabolism of glycerol

A

glycerol kinase

Converts glycerol to glycerol phosphatw

35
Q

glycerol phsophate

A

1) Can be converted to DHAP and used in glycolysis to produce some ATP and reducing power (NADH/FADH2)
2) Or be used in the synthesis of triglycerides

36
Q

acetyl coA is the main

A

convergence point for catabolic pathways

37
Q

Acetyl CoA function

A

act as an important intermediate in both catabolic and anabolic pathways

38
Q

ketones are

A

water soluble molecules, which are alternative substrates to glucose and fatty acids

39
Q

three types of ketone body synthesised in there liver mitochondria (from fatty acids)

A
  1. Acetoacetate (liver)
  2. Acetone
    o Spontaneous decarboxylation of acetoacetate
  3. B-hydroxybutyrate (liver)
40
Q

normal plasma ketone conc

A

<2mM

41
Q

starvation plasma ketone body (physiological ketosis)

A

2-10mM

42
Q

untreated type 1 diabetes (pathological ketosis)

A

> 10mM

43
Q

stains inhibit the enzyme

A

HMG-CoA

44
Q

HMG-CoA reductase catalyses

A

production of cholesterol from acetyl coA

45
Q

Ketoacidosis

A
  • characteristic smell of acetone on breath when acetone excreted via the lungs
  • Acetoacetate and B-hydroxybutyrate are strong organic acids.
46
Q

ketones above renal threshold

A

excreted in the urine (Ketonuria)

47
Q

Regulation of ketone body synthesis by insulin/glucagon (fed/starved) ratio
- Ketone bodies and early starvation:

A

Ketones spare glucose in early starvation/diabetes

  • release of glucagon in reaction to starvation (increase ketone bodies production)
  1. Triglycerides go through lipolysis to produce fatty acids which are released from adipose tissue
  2. These circulate to the liver where the fatty acids undergo ketogenesis where ketone bodies are produced
  3. Ketone bodies are broken down to acetyl CoA where they are used to produce ATP via the TCA and ETC
48
Q

Regulation of ketone body synthesis by insulin/glucagon (fed/starved) ratio
- ketone bodies in well fed state

A

release of insulin’s stimulates production of cholesterol from acetyl CoA

49
Q

in late starvation

A
  1. Protein from muscles are hydrolysed to amino acids
  2. Amino acids circulate to the liver where they are converted to pyruvate
  3. Pyruvate goes through gluconeogenesis to produce glucose
  4. Glycogen in the liver is hydrolysed to produce more glucose
  5. Circulating glucose used to power the brain

Medical Cell Biology and Genetics (33 decks)

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