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Foundations of Medicine > Lipids > Flashcards

Lipids Flashcards

1
Q

What are lipids?

A

Heterogeneous organic molecules

Insoluble in water (hydrophobic), soluble in organic solvents

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2
Q

Where do lipids exist?

A

Exist in cell membranes, as lipid droplets in adipose tissue, in blood lipoproteins

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3
Q

Biological functions of lipids

A
  • Stored form of energy
  • Structural element of membranes
  • Enzyme cofactors
  • Steroid Hormones
  • Vitamins A,D,E,K
  • Signalling molecules
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4
Q

What are the major lipid classes?

A
  • Fatty acids
  • Triacylglycerol
  • Phospholipid
  • Glycolipids
  • Steroid
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5
Q

What are fatty acids?

A

Fatty acids are carboxylic acids that are structural components of fats, oils, and all other categories of lipids, except steroids.

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6
Q

Discuss the structure of fatty acids

A

Straight chain of an even number of carbon atoms, with hydrogen atoms along the length of the chain and at one end of the chain and a carboxyl group (―COOH) at the other end.

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7
Q

What is an unsaturated fatty acid?

A

One or more double bonds in hydrocarbon chain

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8
Q

What is a saturated fatty acid?

A

Are solid, no double bonds in hydrocarbon chain

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9
Q

What are essential fatty acids?

A

Fatty acids that our body cannot produce and we must get them from plants

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10
Q

What are the names of the essential fatty acids?

A

Linoleic acid (LA) - omega-6 family

Alpha linolenic acid (ALA) - omega-3 family

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11
Q

What are good fats?
(cardiovascular)

A

High in polyunsaturated fatty acids: e.g vegetable oils, like olive oil, sunflower oil, ect

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12
Q

What are bad fats?
(cardiovascular)

A

High in saturated fatty acids: (e.g stearic beef) (Saturated - huge role in myelination of nerve fibres and hormone production important in maintaining health)

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13
Q

What are really bad fats?

A

Trans fatty acids, result from hydrogenation of vegetable oils e.g hard margarine (man-made)

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14
Q

What does 18:0 mean?

A

Contains 18 carbons and no double bonds

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15
Q

What does 18:1 mean?

A

18 carbons and one double bond

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16
Q

What can humans not digest?

A

Humans cannot introduce double bonds beyond carbon 9

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17
Q

What is arachidonic acid?

A

A precursor of eicosanoids can be synthesized from linoleic acid

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18
Q

What are omega-3 fatty acids derived from?

A

Omega-3 fatty acids are derived from linolenic acid as essential FAs.

E.g., eicosapentaenoic and docosahexaenoic acid

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19
Q

What does omega 3-FA do?

A

Lowers plasma cholesterol prevents atherosclerosis, lowers TAG prevents obesity, reduces inflammation.

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20
Q

What does omega-6 FA do?

A

Omega-6 FA derived from linoleic areessential but not same benefits

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21
Q

What are triacylglycerols (TAG)?

A

Esters of FAs and glycerol

Esters are neutral uncharged lipids

Dietary fuel and insulation

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22
Q

Discuss TAG and water

A

Water insoluble TAG coalesce into lipid droplets in adipose tissue (major lipid component of adipose tissue)

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23
Q

What are phospholipids?

A

Composed of glycerol bonded to two fatty acids and a phosphate group.

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24
Q

What is the main dietary lipid?

A

Triacylglycerol main dietary lipid

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25
Q

Where is the main site of lipid digestion?

A

Small intestine

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26
Q

What is lipid digestion by pancreatic enzymes (lipases) promoted by?

A

Promoted by emulsification (dispersion) by bile salts and peristalsis (mixing)

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27
Q

What are bile salts?

A

Bile salts are also biologic detergents that enable the body to excrete cholesterol and potentially toxic compounds (eg, bilirubin, drug metabolites).

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28
Q

What is the function of bile salts?

A

Solubilize ingested fat and fat-soluble vitamins, facilitating their digestion and absorption.

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29
Q

What effect does bile salts have?

A

Emulsification of lipids (breaks down fat globules into smaller droplets) - larger surface area for lipase to act on

Forms mixed micelles

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30
Q

What physical mechanism helps with protein digestion?

A

Peristalsis

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31
Q

What are bile salts derived of?

A

Cholesterol

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32
Q

What are micelles?

A

The end product of fat digestion is converted into these.

They are small water soluble droplets.

Fatty acid core and a polar surface

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33
Q

How do we digest triacyglycerols?

A

Most TAG degraded in small intestine by pancreatic lipase to monocyglycerol + two FA

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34
Q

How Do We Digest Cholesterol Esters?

A

Cholesterol esters digested to cholesterol and free FA

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35
Q

How do We Digest Phospholipids?

A

Phospholipids hydrolysed to FA and lysophospholipid.

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36
Q

What does lipid malabsorption cause?

A

Lipid malabsorption due to defects in bile secretion, pancreatic function or intestinal cell uptake results in steatorrhea.

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37
Q

What type of fatty acid chains do not need micelles for absorption?

A

Short and medium chain FA

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38
Q

What is steatorrhea?

A

Steatorrhea is excess fat in faeces. Stools float due to excess lipid, have an oily appearance and are foul smelling.

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39
Q

What secretes bile?

A

Gallbladder secretes bile. Removal of the gallbladder inhibits digestion and absorption of fats

40
Q

What is a chylomicron?

A

A droplet of fat present in the blood or lymph after absorption from the small intestine.

41
Q

Where is lipoprotein lipase?

A

Found primarily in capillaries of skeletal muscle and adipose tissue

42
Q

What happens to free FA?

A

Resulting free FA used for energy or re-esterified to TAG for storage

43
Q

What happens to chylomicrons depleted of TAG?

A

Called chylomicron remnants – go to liver

44
Q

What is glycerol used for?

A

Glycerol is used by liver to produce glycerol-3-phosphate (glycolysis & gluconeogenesis)

45
Q

Storage of TAG

A

In adipose cells TAG are stored as droplets that constitute the “depot fat”

46
Q

Where are fatty acids released from?

A

Released from stored TAG by hormone sensitive lipase (HSL)

47
Q

How is free fatty acid transported through blood?

A

In complex with serum albumin

Albumin most abundant plasma protein with 2-7 binding sites for FA

Most FA esterified (>90%)

These carried in lipoproteins

48
Q

What are the hydrophobic cores of lipoproteins?

A

TGs, cholesteryl esters cores

49
Q

What are the hydrophilic surfaces of lipoproteins?

A

Unesterified cholesterol, phospholipids , apolipoproteins e.g.B100

50
Q

What is good cholesterol?

A

HDL

51
Q

What is bad cholesterol?

A

LDL

52
Q

What does B-oxidation of fatty acids do?

A

Degrades fatty acids to two carbons at a time

53
Q

What does B-oxidation of fatty acids produce?

A

Acetyl CoA and NADH and FADH2 which are sources of energy (ATP)

54
Q

What are the three stages in B-oxidation fatty acid?

A
  1. Activation of fatty acids in the cytosol
  2. Transport into the mitochondria
  3. Degradation to two carbon fragments as acetyl CoA in the mitochondrial matrix - energy
55
Q

What is fatty acid activated to form?

B-oxidation

A

Fatty acid acyl CoA in cytoplasm.

56
Q

How does long chain fatty acid acyl CoA get into mitochondrial matrix for oxidation?

A

Via citrate shuttle

57
Q

Where is fatty acid transported to?

A

Transport activated fatty acid into the mitochondira, the inner mitchondrial matrix.

58
Q

When does the citrate shuttle occur?

A

When citrate concentration in mitochondria is high

59
Q

What happens once citrate is in the cytosol?

A

Citrate lyase releases the acetyl CoA and combines on a CoA part in the cytosol and forms oxaloacetate.

Aceytl CoA now in cytosol ready for fatty acid synthesis.

60
Q

What enzymes are needed for fatty acid synthesis?

A

Acetyl CoA carboxylase (Activation/regulation - really important rate limiting step)

Fatty acid synthase (multifunctional enzyme)

61
Q

What is CAT-1 needed for?

A

FA synthesis

Inhibited by malonyl CoA

62
Q

What does the citrate shuttle prevent?

A

Prevents synthesis and degradation occuring simultaneously

63
Q

Where do we get carnitine?

A

Carnitine from diet or made from lysine or methionine (liver/kidney)

64
Q

Discuss CAT-1 deficiency

A
  • No B-oxidation, hypoglycemia
  • Coma on overnight fast
  • Improved with IV glucose
  • Therapy - give medium chain fatty acids that do not require CAT for mitochondrial transport
65
Q

What is needed for the fatty acid to be synthesised?

A

Acetyl CoA
(NADH reduced to form) NADHP

66
Q

What is the main product of fatty acid synthesis?

A

Palmitic acid (16 carbon fatty acid often called palmitate)

67
Q

What activates acetyl-CoA carboxylase?

A

Citrate

Signals that there is enough glucose so make FA

68
Q

What deactivates acetyl-CoA carboxylase?

A

Palmitoyl CoA

Enough FA made so halt synthesis

Gulcagon, epinephrine deactivates

69
Q

Overall reaction for fatty acid synthesis

A

8 acetyl CoA + 14 NADPH + 14 H+ + 7ATP

——–>

Palmitate + 8 CoA + 14 NADP+ + 7ADP + 7P + 7H2O

70
Q

Where does any further modification of palmitate or dietary FAs (unsaturation, elongation, branching) occur?

A

Occurs in mitochondria and ER by diverse enzymes

71
Q

Can essential fatty acids be synthesised?

A

No but are required to make other lipids

72
Q

Fate of fatty acid

A

Acetyl CoA –> Fatty Acid (liver) —> (glycerol -P) TAG –> (protein phospholipid cholesterol) –> VLDL –> Adipose tissue

73
Q

Degradation of free fatty acid

A
  1. Dehydrogenation to produce FADH2
    - aka oxidation FAD to FADH2 for ATP formation
  2. Hydration
    - Requires H2O

3.. Dehydrogenation to produce NADH
- aka oxidation NAD+ to NADH for ATP formation

  1. Thiolysis (cleaved) to produce acetyl CoA to feed into the TCA cycle
74
Q

Energy formed during B-oxidation of fatty acids?

A

129

75
Q

Where does B-oxidation of very long fatty acids happen?

A

Very long chain fatty acids» 22 carbons undergo a preliminary B-oxidation in peroxisomes

76
Q

What are ketones?

A

Fuel molecules (good)

77
Q

What happens during fasting or starvation?

A

Glucose is decreased and excess acetyl CoA from fat metabolism can be converted to ketone bodies

78
Q

What use ketone bodies as energy?

A

-Cardiac and skeletal muscles

  • Ketone bodies can fuel brain cells during starvation (brain cannot use FA as fuel source)
79
Q

Where are ketone bodies formed?

A

In the liver (mitchondrial matrix) and is transported with the blood to other cells where it is used as fuel

80
Q

Can the liver use ketone bodies?

A

Liver makes but cannot use ketone bodies

81
Q

Ketone bodies and acetyl-CoA

A

Water soluable transporters of acetyl-CoA

82
Q

What do excessive ketone bodies?

A

Uncontrolled diabetes or starvation leads to very high ketone body concentrations in the blood

When the rate of ketone body production exceeds utilisation, ketonemia (blood KB) ketonruia (urine KB) and acidemia results

Fruity odour in breath due to acetone results

83
Q

What is diabetic ketosis when insulin was absent?

A

Decrease insulin, increased glucagon - increased lipolysis - increased free fatty acids in plasma - increased hepatic output of ketone bodies - increased ketoacidosis

84
Q

Where can we get fatty acids from?

A

Our diet (essential)
Synthesis - from excess carbohydrate, fat and protein compounds (acetyl CoA)

85
Q

Where does fatty acid synthesis occur?

A

Fatty Acid Synthesis occurs in:

  • Liver
  • Lactating mammary gland
  • Adipose tissue
86
Q

What are fatty acids synthesised from?

A

Acetyl CoA

87
Q

What does the synthesis of fattu acid need?

A

Uses ATP and NADPH

88
Q

What are the enzymes of fatty acid synthesis?

A
  • Acetyl CoA carboxylase (Activation/regulation)
  • Fatty acid synthase (multifunctional enzyme)
89
Q

What is the product of fatty acid synthesis?

A

Palmitic acid

90
Q

What metabolic and hormonal signals control the activity of acetyl-CoA carboxylase?

A

Acetyl-CoA carboxylases

ACC - key regulatory enzyme activated by citrate and deactivated by palmitoyl CoA - synthesises malonyl CoA

91
Q

What activates Acetyl-CoA carboxylases?

A

Activated by citrate (signals that there is enough glucose - so makes FA)

Insulin activates glucagon

92
Q

What deactivates Acetyl-CoA carboxylases?

A

Deactivated by palmitoyl CoA (enough fatty acid made so half synthesis)

Epinephrine deactivates

93
Q

What forms acetoacetyl-ACP and what drives this reaction?

A

Acyl-malonyl ACP condensing (bond forming) enzyme forms acetoacetyl-ACP

This reaction is driven by the decarboxylation

94
Q

Steps on reduction-dehydration-reduction

A

FA cleavage
Acyl carrier protein
14 NADPH for Palmitate Synthesis

95
Q

Where does any further modification of palmitate or dietary Fas (e.g. unsaturation, elongation, branching) take place?

A

In mitochondria and ER by diverse enzymes

Foundations of Medicine (56 decks)

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