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Science for Medicine > Lipids > Flashcards

Lipids Flashcards

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Biology 101 flashcards
1
Q

What are lipids?

A
  • Heterogeneous organic molecules
  • Insoluble in water (hydrophobic) but soluble in organic solvents
  • Exist in cell membranes, as lipid droplets in adipose tissue, in blood lipoproteins
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2
Q

Biological functions of lipids

A
  • Stored form of energy
  • Structural element of membranes
  • Enzyme cofactors
  • Hormones
  • Vitamins A,D,E,K
  • Signalling molecules
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3
Q

Digestion and absorption of lipids

A
  • Triacylglycerol main dietary lipid
  • Others: phospholipids, cholesterol, cholesterol ester, free fatty acids
  • Small intestine main site of digestion
    Lipid digestion by pancreatic enzymes (lipases) is promoted by emulsification (dispersion) by bile salts and peristalsis (mixing)
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4
Q

Fatty acid nomenclature

18:0

A

contains 18 carbons and no double bonds

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5
Q

Essential fatty acids are

A

Linoleic and a-linolenic; must get these from plants

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6
Q

“bad fats (cardiovascular)” are

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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7
Q

“really bad fats”:

A

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

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8
Q

What are Essential fatty acids?

A
  • Linoleic and linolenic acids are essential FA in humans
  • Humans cannot introduce double bonds beyond carbon 9
  • Must ingest essential FA

Arachidonic acid, a precursor of eicosanoids can be synthesized from linoleic acid

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9
Q

Omega (w)-3 fatty acids are derived from

A

linolenic acid as essential FAs.
E.g., eicosapentaenoic and docosahexaenoic acid

  • Omega-3 FA lowers plasma cholesterol prevents atherosclerosis, lowers TAG prevents obesity, reduces inflammation.
  • Omega-6 FA derived from linoleic are essential but not same benefits (???)
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10
Q

essential fatty acid deficiency symptoms

A
  • Growth retardation
  • Reproductive failure
  • Skin lesions
  • Kidney and liver disorders
  • Subtle neurological and visual problems
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11
Q

essential fatty acid (omega 3) deficiency can lead to

A

depression
- inadequate intake alters brain activity or depression
alters fatty acid metabolism?
Attention deficit hyperactivity disorder
- lower levels of omega 3 cause more behavioural
problems

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12
Q

Triacylglyerols (TAG)(Triglycerides) are

A

Esters of fatty acids and glycerol

  • Esters are neutral uncharged lipids
  • Water insoluble TAG coalesce (come together) into lipid droplets in adipose tissue (major lipid component of adipose tissue)
  • Dietary fuel and insulation
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13
Q

Phospholipids are composed of

A

glycerol bonded to two fatty acids and a phosphate group.
- Amphipathic - charged phosphate group as ‘head’ of a phospholipid is hydrophilic (attracted to water) whereas the hydrophobic ‘tails’ repel water.

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14
Q

main site of lipid digestion is

A

small intestine

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15
Q

main dietary lipid is

A

triacylglycerol

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16
Q

lipid digestion by pancreatic enzymes (lipases) is promoted by

A

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

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17
Q

bile salts act as

A
  • biological detergents to form emulsions and mixed micelles
  • Saves lipids coalescing (coming together) in an aqueous environment
  • Derivatives of cholesterol
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18
Q

bile salt are made up of cholic acid and

A
  • taurine which made taurocholic acid
  • glycine which made glycocholic acid

both are major bile salts

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19
Q

How do we digest triacylglycerols?

A

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

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20
Q

Digestion of cholesterol esters (and phospholipids)

A
  • Cholesterol esters digested to cholesterol and free FA

- Phospholipids hydrolysed to FA and lysophospholipid

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21
Q

fat gets converted into

A

emulsified fats (through bile) and then fatty acids and glycerol (through lipase)

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22
Q

Uptake of digested lipids:

- Products of lipid digestion form

A

mixed micelles with bile salts.
Mixed micelles approach brush border membranes of enterocytes and release lipid products which enter cells by diffusion.
Short and medium chain FA do not require micelles for absorption

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23
Q

What is Steatorrhea?

A

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

  • Steatorrhea is excess fat in faeces. Stools float due to excess lipid, have an oily appearance and are foul smelling
  • Gallbladder secretes bile. Removal of the gallbladder inhibits digestion and absorption of fats
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24
Q

Cystic fibrosis patients are prone to

A

steatorrhea as with their thickened pancreatic secretions, pancreatic enzymes are less able to reach the small intestine which is the primary site of lipid digestion

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25
Q

Utilisation of dietary lipids

What happens to absorbed fatty acids?

A

Intestinal cells resynthesize TAG, PL, CE for export
- insoluble so packaged with apoB-48 (solubilising protein) into chylomicrons for export

Chylomicrons are released by exocytosis into lymph then blood

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26
Q

What happens when blood chylomicrons reach tissue?

A

TAG in chylomicrons is hydrolysed to FA and glycerol by lipoprotein lipase
Lipoprotein lipase is found primarily in capillaries of skeletal muscle and adipose tissue

Resulting free FA used for energy or re-esterified to TAG for storage
Chylomicrons depleted of TAG are called chylomicron remnants – go to liver
Glycerol is used by liver to produce glycerol-3-phosphate (glycolysis & gluconeogenesis)

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27
Q

step 1 :

bile salts emulsify dietary fats in the

A

small intestine forming mixed micelles.

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28
Q

step 2:

intestinal lipases

A

degrade triacylglycerols

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29
Q

step 3:

fatty acids d other breakdown taken products are taken up by the

A

intestinal mucosa and converted into triacylglycerols

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30
Q

step 4:

triacylglycerols are incorperated with

A

cholesterol and apolipoproteins into chylomicrons.

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31
Q

step 5:

chylomicrons move through

A

the lymphatic sytstem and bloodstream to tissues

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32
Q

step 6:

lipoprotein lipase is activated by

A

apoC-II in the capillary.

converts triacylglycerol into fatty acids and glycerol

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33
Q

step 7:

fatty acids enter

A

cells

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34
Q

step 8:

fatty acids are

A

oxidised as fuel or reesterified for storage

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35
Q

Synthesis and storage of TAG

A
  • In adipose cells TAG are stored as droplets that constitute the “depot fat”
  • TAG is the most efficient storage form of fuel (highly reduced, nearly anhydrous (containing no water))
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36
Q

fatty acids are released by

A

lipoprotein lipase.

fatty acids are released when energy supply is low.

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37
Q

How are FA released from stored TAGin adipose tissue?

A
  • FA released from stored TAG by hormone sensitive lipase (HSL)
  • HSL activated by phosphorylation in response to epinephrine (aka adrenaline)
  • High plasma glucose and insulin promote dephosphorylation (inactivation) of lipase
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38
Q

How are FA transported in blood?

A
  • Free FA transported through blood 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
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39
Q

Lipoproteins

A

TAGs, and cholesterol esters are insoluble in water and cannot be transported in blood or lymph as free molecules

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40
Q

lipoproteins are made up of

A

cholesteryl ester
phospholipid
unesterified cholesterol
apolipoprotein B-100

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41
Q

Lipoproteins

Hydrophobic cores :

A

TGs

cholesteryl esters cores

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42
Q

Lipoproteins

Hydrophilic surfaces :

A

unesterified cholesterol
phospholipids
apolipoproteins e.g.B100

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43
Q

Lipoprotein classes

A

Chylomicrons
VLDL
LDL
HDL

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44
Q

Lipoprotein classes

A

Chylomicrons
VLDL
LDL
HDL

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45
Q

Lipoprotein

Classified according to density (least to most)

A 
- Chylomicrons –TAG rich 
     (TAG from intestine to tissues). 
- VLDL –TAG rich
     (TAG from liver to tissue)
- LDL – cholesterol rich
     (cholesterol to extrahepatic tissue – BAD cholesterol) 
- HDL – protein/cholesterol rich. 
      (Transports cholesterol from tissue to liver for 
       elimination– GOOD cholesterol)
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46
Q

LDL provides cholesterol to

A

peripheral tissues.
Too much LDL results in too little uptake and the protein on LDL becomes modified.
When this happens macrophages in arteries form foam cells and atherosclerotic plaques.

HDL sucks cholesterol out of the plaque and also provides cholesterol to the liver for bile synthesis and hormone synthesis.

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47
Q

As VLDL passes through the circulation, TAG

A

is degraded by lipoprotein lipase and VLDL converted to LDL.

48
Q

Fatty acids cannot be

A

converted to glucose

49
Q

Release of FA from TAG in adipocyte:

The free unesterified fatty acid leaves the

A

adipocyte and binds to albumin.

It is transported to tissue, activated to CoA derivitive then oxidised

50
Q

The β-oxidation pathway

A

fatty acids two carbons at a time
Produces acetyl CoA and also NADH and FADH2 which are sources of energy (ATP)
- Occurs in mitochondrial matrix

51
Q

What happens in b-oxidation?

A

there are three stages:

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!

52
Q

in beta oxidation Fatty acid is activated to form

A

fatty acyl CoA in cytoplasm.

this is done by acyl CoA synthase

53
Q

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

A

Transport by Carnitine Shuttle

  • Major site of regulation
  • Carnitine fatty acyl-transferase (CAT-1) or Carnitine palmitoyl-transferase is inhibited by malonyl CoA (needed in FA synthesis)
  • Prevents synthesis and degradation occurring simultaneously
  • Carnitine from diet or made from lysine or methionine (liver/kidney)
54
Q

Carnitine fatty acyl-transferase (CAT-1) or Carnitine palmitoyl-transferase is inhibited by

A

malonyl CoA (needed in FA synthesis)

55
Q

Carnitine palmitoyl-transferase (or CAT-1) deficiency

A

No b-oxidation causes hypoglycemia
Coma on overnight fast
Improved with iv glucose

Therapy -Give medium chain FA that does not require CAT for mitochondrial transport

56
Q

A carnitine-associated defect in

A

liver fatty acid b-oxidation impairs the liver’s capacity to use fatty acids as fuels, and puts an extra burden on its capacity to generate glucose through gluconeogenesis.

For deficiency in muscle, avoid too much strenuous exercise and excessive fat in the diet

57
Q

Degradation in b-oxidation contains 4 main steps

A
  • Dehydrogenation to produce FADH2 (oxidation of FAD to form FADH2 to form ATP formation)
  • Hydration (requires H2O)
  • Dehydrogenation to produce NADH (oxidation of NAD+ to form NADH to form ATP formation)
  • Thiolysis (cleaved) to produce acetyl CoA to feed into the TCA cycle
58
Q

medium chain fatty acyl CoA dehydrogenase deficiency is a

A

common inborn error of metabolism

59
Q

Result from palmitate (16:0)

A

Each b-oxidation cycle -One acetyl CoA and a species two carbon atoms shorter than the original

Therefore 7 β-oxidations produces 8 acetyl CoA + 7 FADH2 + 7 NADH

60
Q

What is energy yield?

palmitate (16:0)

A 
FADH2 – 2 ATP		x 7 = 14
NADH – 3 ATP 		x 7 = 21
Acetyl CoA – 12 ATP	x 8 = 96
TOTAL			              = 131

2 ATP are needed in production of palmitoyl CoA, so

TOTAL = 129 ATP
(32 ATP from 1 glucose molecule)

61
Q

b-oxidation in the peroxisome

A
  • Very-long chain fatty acids >22 carbons undergo a preliminary b-oxidation in peroxisomes.
  • First step does not produce FADH2 and so less energy efficient
  • The shortened FA linked to carnitine diffuses from peroxisome into the mitochondria for further oxidation.
62
Q

Defects in b-oxidation in the peroxisome results in

A

VLC-FA accumulation in blood and tissue

63
Q

Animals CANNOT convert

A

FA to glucose(no fatty acid is gluconeogenic).

- Cannot convert acetyl CoA into glucose due to thermodynamically irreversible pyruvate to acetyl CoA step- (Important)

64
Q

What happens to excess acetyl CoA from FA degradation?

A

gets converted into ketone bodies during fasting or starvation.
- Acetyl CoA INHIBITS pyruvate dehydrogenase,
ACTIVATES pyruvate carboxylase
- oxaloacetate gets converted to glconeogenesis

65
Q

The amount of ketogenesis depends on

A

the availability of acetyl CoA

66
Q

Ketone Bodies Are

A

Fuel Molecules (good)

67
Q

During fasting or starvation, glucose is

A

decreased, and excess acetyl CoA from fat metabolism can be converted to ketone bodies:

  • Cardiac and skeletal muscles use ketone bodies as an energy source.
  • Ketone bodies can fuel brain cells during starvation
    (Brain cannot use FA as fuel source)
68
Q

Ketone bodies are formed in

A

liver (mitochondrial matrix) and is transported with the blood to other cells where it is used as fuel.
- Liver makes but cannot use ketone bodies

69
Q

Ketone Bodies Are

A 
Fuel Molecules (good)
water-soluble transporters of Acetyl-CoA
70
Q

Excessive ketone bodies (bad!)

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), ketonuria (urine KB) and acidemia results - blood ph can drop.

  • Fruity odour in breath due to acetone results
71
Q

Ketone bodies are soluble in

A

blood- do not need albumin or lipoprotein

72
Q

Diabetic ketosis results when

A

insulin is absent as glucose in blood is not detected by adipose tissues or liver.

Due to a lack of glucose-derived oxaloacetate citric acid slows down, Ac-CoA cannot be processed after β-oxidation.

73
Q

FA synthesis and degradation

A

donot run at the same time

74
Q

FA-degradation

A 
Mito matrix
CoA
Multiple enzymes
Ac-CoA
NAD+, FAD
75
Q

FA synthesis and degradation

A

donot run at the same time as it would be a wast of energy if it did

76
Q

FA-degradation

A 
occurs in Matrix of mitochondria
carrier protein is CoA
Multiple enzymes
building block is Ac-CoA
NAD+, FAD (oxidant)

(cleavage)

77
Q

FA-synthesis

A 
occurs in Cytosol
carrier protein is ACP
Enzyme complex
building block is Mal-CoA
NADPH  (reductant)

(condensation)

78
Q

acetyl CoA cannot permeate

A

to the inner membrane so transferase turns this into fatty acyl carnitine so it can permeate.
transaceylation takes place again forming Acetyl CoA in the matrix space.

79
Q

Fatty acid synthesis occurs in …

A

Liver
Lactating mammary gland (breast)
(Adipose tissue)

80
Q

Where do we get fatty acids?

A

Diet (essential fatty acids)

Synthesis - from excess carbohydrate and protein components (acetyl CoA)

81
Q

De novo synthesis of Fatty acids is when

A

FA is synthesised from acetyl CoA, derived from excess protein, fat and carbohydrate

  • Uses ATP and NADPH
  • Occurs in cytosol

Acetyl CoA is formed in mitochondria and so needs to be transferred to cytosol

82
Q

Fatty Acid Synthesis Occurs in the

A

Cytosol from acetyl CoA in mitochondria.

CoA cannot cross mitochondrial membrane (only “acetyl” part can cross)

83
Q

Citrate shuttle occurs when

A

citrate concentration in mitochondria is high

84
Q

Fatty acid synthesis Enzymes

A

Acetyl CoA carboxylase (activation/regulation)

Fatty acid synthase (multifunctional enzyme)

85
Q

Fatty acid synthesis Needs

A

Acetyl CoA and NADPH

86
Q

Fatty acid synthesis Product

A

Palmitic acid

87
Q

Acetyl CoA Carboxylase needed for

A

Formation of Malonyl CoA-activation step.

  • Formation of malonyl–CoA is the committed step in fatty acid synthesis.
  • C-C bond needs much energy- energy supplied indirectly by synthesising malonyl CoA
88
Q

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

A

ACC- key regulatory enzyme

  • activated by citrate (signals that there is enough glucose and so makes FA)
  • deactivated by palmitoyl CoA (enough fatty acid made so halt synthesis)

Insulin activates, glucagon, epinephrine deactivates

89
Q

Acetyl Co A carboxylase- regulation

A

ACC- key regulatory enzyme, activated by citrate and deactivated by palmitoyl CoA (short term)
Insulin activates, glucagon, epinephrine deactivates

90
Q

Elongation is when Acyl-malonyl ACP condensing (bond forming) enzyme forms

A

Acetoacetyl-ACP

91
Q

Reduction-dehydration-reduction

The next three reactions are similar to the reverse of fatty acid degradation, except

A

The NADPH is used instead of NADH and FADH2

92
Q

FA cleavage

A

The elongation cycle is repeated six more times, using malonyl–CoA each time, to produce palmityl–ACP.

A thioesterase then cleaves the palmityl–CoA from the ACP.

93
Q

Acyl Carrier Protein (ACP)

The intermediates in fatty acid synthesis are

A

covalently linked to the acyl carrier protein (ACP)

94
Q

The pantothenate arm of the ACP

A

moves the intermediates form one active site to the next.

95
Q

14 NADPH for

A

palmitate synthesis

  • Pentose phosphate pathway (6NADPH)
  • Malic enzyme reaction that converts malate to pyruvate (8NADPH)
96
Q

Elongation and desaturation

A

Any further modification of palmitate or dietary FAs (e.g. unsaturation, elongation, branching) occurs in mitochondria and ER by diverse enzymes

NB essential fatty acids cannot be synthesised but are required to make other lipids (eicosanoids)

97
Q

fatty acid synthesis involves

A

condensation, reduction, dehydration, reduction

98
Q

fatty acid degradation involves

A

dehydrogenation, hydration, dehydrogenation, thiolysis

99
Q

Steroids and Eicosanoids are

A

specialised lipid classes

100
Q

Steroid hormones are

A

chemical substances that serve as chemical messengers in the body (glucocortocoids, mineralocortocoids, sex hormones.
steroids have 4 carbon rings

101
Q

Cholesterol is the

A

starting material for the synthesis of steroid hormones.

102
Q

Eicosanoids are derived from

A

20-carbon unsaturated fatty acids (eicosanoic acids) and are synthesised throughout the body

103
Q

sterols: cholesterol

function

A 
component of cell membrane
precursor to other substances
      - sterol hormones
      - vitamin d
      - bile acids (help digest fats)
104
Q

sterols: cholesterol

synthesis

A

mainly in the liver

105
Q

sterols: cholesterol

food sources

A

found only in animal foods

106
Q

cholesterol is used in

A 
bile salts
membranes
plasma lipoproteins
modify proteins
vitamin D
Steroid hormones
107
Q

Statins function - cholesterol

A

Inhibit HMG-CoA reductase that is essential in cholesterol synthesis
Lower LDL levels
Improve risk of developing cardiovascular disease

108
Q

Eicosanoids are signaling molecules derived from

A

omega-3 or omega-6 fatty acids.

Precursors to prostaglandins, thromboxanes, and leukotrienes.

  • Exert control over inflammation or immunity, and as messengers in the central nervous
  • Short half life
109
Q

Eicosanoids regulate…

A

Inflammatory response (joints, skin, eyes)

  • Pain & fever (Prostaglandins)
  • Many reproductive functions (e.g. labour induction) & menstrual cramps (prostaglandins)
  • Blood pressure regulation (prostacyclin)
  • Blood clotting induction (thromboxanes)
  • SMC constrictions & broncioconstriction (leukotrienes)
110
Q

Eicosanoid analogues in medicines.

A

Montelukast and Zafirlukast ( Leukotriene antagonists) asthma treatment (inhibit leukotrienes).

Carboprost (Prostaglandin analog) induces labor.

111
Q

COX inhibitors are

A

Anti-inflammatory and fever-reducing property of aspirin due to inhibition of COX1 enzyme and prostaglandin synthesis.

112
Q

Aspirin inhibits

A

thromboxanes that cause clotting –given to susceptible patients

113
Q

FAS is a

A

multifunctional enzyme

114
Q

Citrate moves acetyl CoA

A

from mitochondria to cytosol

115
Q

FA synthesis occurs in

A

cytosol of liver from acetyl CoA

116
Q

Eicosanoids are precursor for

A

prostaglandins, thromboxanes and leukotrienes

Science for Medicine (16 decks)

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