Fatty acids Flashcards

1
Q

What is the general structure of NEFA?

A

alkyl with a carboxyl end

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2
Q

What happens to the melting point and the hydrophobicity as the fatty acid chain increases in length?

A

the greater the length the greater the melting point

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3
Q

What is meant by a saturated long chain FA?

A

no C=C bonds

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4
Q

Where does the position of the w or n bond start from in the omega naming system?

A

begins from the alkyl end

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5
Q

Where does the positon of the delta bond originate from when using the delta system?

A

originates from the carboxyl end

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6
Q

What happens to the melting point as we add more C=C double bonds?

A

melting point lowers

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7
Q

What type of isomer are natural unsaturated fatty acids?

A

cis isomers

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8
Q

What type of isomer typically has a flat structure?

A

trans isomers

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9
Q

What are the 2 main states that fatty acids can exist in animals?

A

Bound to albumin or esterified

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10
Q

What is an esterification reaction

A

Refers to the reaction between an alcohol (OH) and a organic acid (COOH)

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11
Q

What is the function of TAG?

A

storage form of fat and also a transport form of fat

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12
Q

What is unique about phospholipids when comparing them to TAG?

A

3rd bond is with a polar group (often with Pi)

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13
Q

What is the fat yield in comparison to glucose dry weight?

A

2 times more (fat)

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14
Q

What is the fat yield in comparison to glucose in vivo?

A

6 times

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15
Q

What is the time frame of fat compared to glycogen?

A

glycogen is one to two days, fat is about 6 weeks

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16
Q

When does exercise utilise the most amount of fat?

A

utilises fat most at around 50% of VO2 max

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17
Q

What are the three steps involved in the oxidative process?

A
  1. TAG to NEFA
  2. Activation and transport
  3. B oxidation
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18
Q

Where is TAG converted to NEFA?

A

Adipose tissue and in the capillary wall

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19
Q

Where is hormone sensitive lipase, what is its function and when is it most active?

A
  • adipose tissue
  • get NEFA out of the adipose tissue
  • HSL is active in fasted state
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20
Q

Where is lipoprotein lipase and when is it most active?

A
  • blood/capillary walls
  • LPL gets NEFA into the cells
    LPL is active in the fed state (low Km and is hence always active with the substrate)
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21
Q

Describe the form of TAG within the blood:

A
  • form of water soluble lipoproteins

- non-lipid core surrounded by phospholipid

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22
Q

What type of lipoprotein transports TAG from the gut to the tissues?

A

Chylomicrons

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23
Q

What type of lipoprotein transports from the liver to the tissues?

A

Very low density lipoproteins

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24
Q

Explain how hormone sensitive lipase functions:

A
  1. Hormone receptor is on the adipocyte
  2. Stimulates adenylate cyclase = cAMP
  3. Activates protein Kinase that phosphorylates HSL
  4. PKA also phosphorylates perilippin
  5. Where lipolysis occurs yields NEFA
  6. NEFA leaves adipocyte in blood on serum albumin
  7. Enters target cell and is then oxidised
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25
Q

What is involved in the activation and transport phase of fax oxidation?

A
  1. Formation of acyl CoA from fatty acids to be processed through the metabolism
  2. Transport of acyl CoA into the mitochondria
26
Q

What enzyme is involved in the formation of acyl CoA

A

acyl CoA synthetase

27
Q

What is the name of the acyl CoA transporter

A

carnitine

28
Q

What are the two main important enzymes within the mitochondrial membrane?

A

carnitine palmitoyl trasnferase one and carnitine palmitoyl trasnferase two

29
Q

How is the transport step regulated

A

negatively regulated by malonyl CoA

30
Q

What are the steps that are involved in the synthesis of acetyl CoA?

A
1. Removal of e- (FAD)
add H2O
removal of electrons NAD 
split of acetyl CoA 
2. Oxidation via the TCA cycle
31
Q

What is the yield from C16?

A

106 ATP

32
Q

How is beta oxidation controlled?

A
  • Lipolysis
  • CPT1 and to some extent malonyl CoA
  • Enzymes not rate limiting but rather the number of them
33
Q

What are the constraints of fatty acid oxidation?

A
  • aerobic
  • several tissues cannot use fat
  • limited power
34
Q

How does fat oxidation interlink with other pathways ?

A

Glycolysis- metabolites of fat oxidation inhibit gylcolysis

Long chain fatty acid synthesis- malonyl CoA

35
Q

What is a ketone?

A
  • water soluble 4C acid

- made from 2 acetyl CoA in the liver

36
Q

What are the two main ketone bodies?

A

acetoacetate

D-3-hyrdoxybutyrate

37
Q

Where are ketone bodies regularly used?

A
  • red muscle and the gut to spare glucose
38
Q

What are the ketone decarboxylation products?

A
  • acetone

- isopropanol

39
Q

Where does hepatic ketogenesis occur?

A
  • in the liver mitochondria
40
Q

What does ketogenesis enable the liver to do?

A
  • gain energy from B oxidation
  • Rely less on TCA
  • Rapid uptake of NEFA
41
Q

How is ketogenesis controlled?

A
  • lipolysis
  • high activity of CPT1
  • hormone sensitive lipase
42
Q

Compare physiological and pathological ketosis

A

Physiologcal is when the levels in the blood are not too high and hence ketogenesis allows for the maximum amount of NEFA to be mobilised. Whereas pathological is when concentration is too high resulting in ketoacidosis

43
Q

What is special about primate?

A
  • able to use ketone bodies as brain is large and hence needs an alternative means of fuel
44
Q

Where does lipogenesis occur in pigs and ruminants?

A

Liver

45
Q

Where does lipogenesis occur within a bird?

A

adipose

46
Q

What are the two main needs of lipogenesis?

A

NADPH and acetyl CoA

47
Q

What are the four main steps of lipogenesis?

A
  1. Formation of acetyl CoA in cytoplasm
  2. Acetyl CoA carboxylase
  3. Fatty acid synthase- makes the fatty acid 2 carbons at a time
  4. Provision of reducing power
48
Q

What are the two enzymes in the citrate cleavage pathway?

A
  1. ATP citrate lyase

2. NADH malate dehydrogenase

49
Q

How is the citrate cleavage pathway regulated?

A

Regulated via insulin

50
Q

What is the name of the enzyme that converts acetyl CoA to malonyl CoA?

A

acetyl CoA carboxylase

51
Q

How is acetyl CoA carboxylase regulated?

A
  • activated by insulin, inhibited by glucagon/ adrenalin

- activated by citrate, inhibited by NEFA CoA

52
Q

Where does the reducing power come from for

A

50/50 citrate cleavage and pentose phosphate

53
Q

What is a special enzyme for lipogenesis in ruminants?

A

NADP isocitrate dehydrogenase

54
Q

What do desaturases have?

A

4,5, 6, 9

55
Q

What are the parent fatty acids?

A

linoleic and linolenic acid

56
Q

What are eicosanoids precursors for?

A

prostaglandins and thromboxane platelets

57
Q

What is the function of prostacyclin?

A

vasodilator

58
Q

Is n-3 derived from prostacyclin strong or weak anticlotting?

A

n-3 derived prostacyclin is strong anti-clotting

59
Q

Where does the dietary supply of n-6 FA’s come from?

A
  • oils extracted from plants
60
Q

Where does the dietary supply of n-3 FA’s come from?

A
  • Chloroplasts
  • Plankton/algae
  • Linseed/Canola