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Lipids Flashcards

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1
Q

What are lipids?

A

Heterogeneous organic molecules.

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2
Q

Are lipids soluble in water?

A

No.

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3
Q

Are lipids soluble in organic solvents?

A

Yes.

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4
Q

What are lipids soluble in?

A

Organic solvents.

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5
Q

Where do lipids exist?

A

Cell membranes
Lipid droplets in adipose tissue
Lipoproteins in blood

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6
Q

What do lipids exist as in adipose tissue?

A

Lipid droplets.

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7
Q

What do lipids exist as in the blood?

A

Lipoproteins.

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8
Q

What are the functions of lipids?

A 
Stored form of energy
Structural element of membranes
Hormones
Signalling molecules 
Enzyme cofactors
Vitamins (needed for ADEK function)
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9
Q

What can lipids store?

A

Energy.

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10
Q

What can lipids act as a structural element of?

A

Cell membranes.

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11
Q

What can lipids act as a cofactor for?

A

Enzymes.

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12
Q

What can lipids work as to signal responses?

A

Hormones / signalling molecules.

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13
Q

What vitamin functions are lipids required for?

A

Function of ADEK vitamins.

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14
Q

What do lipid classifications include?

A

Fatty acids, triaceylglycerols, phospholipids, glycolipids and steroids.

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15
Q

What can imbalances/deficiencies in lipid metabolism lead to?

A

Major clinical problems such as atherosclerosis, obesity and metabolic disorder.

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16
Q

What are the 2 types of fatty acid?

A

Saturated

Unsaturated

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17
Q

What characterises saturated fatty acids?

A

No C=C bonds, straight chains, solids.

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18
Q

What characterises unsaturated fatty acids?

A

C=C bonds, kinked chains, liquids.

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19
Q

What is fatty acid nomenclature based on?

A

Number of carbons and bond positioning.

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20
Q

What are ‘good’/’bad’ fatty acids based on?

A

Saturation.

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21
Q

What are good fatty acids high in?

A

Polyunsaturated fats.

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22
Q

What are bad fatty acids high in?

A

Saturated fats.

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23
Q

What do very bad fatty acids result from?

A

Hydrogenation of vegetable oils.

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24
Q

What are essential fatty acids?

A

Essential fatty acids are those which must be ingested in the diet- they are linolenic acids from plants.

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25
Q

What are essential fatty acids called?

A

Linolenic acids.

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26
Q

What are linolenic acids derived from?

A

Plants.

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27
Q

Why must essential fatty acids be ingested?

A

Humans cannot introduce C=C bonds past carbon 9.

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28
Q

What are omega-3 fatty acids?

A

Essential fatty acids which are derived from linolenic acid and work to lower cholesterol and prevent CVDs.

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29
Q

What do deficiencies in essential fatty acids cause?

A

Chronic intestinal disease
Growth retardation
Depression
ADHD

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30
Q

What are triaceylglycerols?

A

Esters of fatty acids and glycerol.

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31
Q

How are triaceylglycerols formed?

A

Esterification.

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32
Q

What charge do triaceylglycerols have?

A

Neutral / no charge.

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33
Q

What do water-insoluble TAGs disperse as in the adipose tissue?

A

Lipid droplets.

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34
Q

What are triaceyglycerols used for?

A

Dietary fuel and insulation.

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35
Q

What are phospholipids composed of?

A

Glycerol bonded to 2 fatty acids and a phosphate head.

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36
Q

Why are phospholipids described as being amphipathic?

A

Dual hydrophilic/hydrophobic nature- the ionic phosphate head is hydrophilic whilst the fatty acid chains are hydrophobic.

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37
Q

What is the main dietary lipid?

A

Triaceylglycerol (TAG).

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38
Q

What other dietary lipids are there?

A

Phospholipids, cholesterol, cholesterol esters and free fatty acids.

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39
Q

What is the main site of lipid digestion.

A

Small intestine.

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40
Q

How are lipids initially digested?

A

Pancreatic lipase.

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41
Q

What is digestion of lipids by pancreatic lipase promoted by?

A

Emulsification.

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42
Q

What is emulsification?

A

Dispersion/mixing.

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43
Q

What are the 2 contributing factors to emulsification which promote lipid digestion?

A

Bile salts

Peristalsis

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44
Q

What are bile salts?

A

Biological detergents- prevent lipids from coalescing in aqueous environments.

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45
Q

What do TAG form following digestion with pancreatic lipase?

A

Monoaceylglycerol and 2 fatty acids.

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46
Q

What do cholesterol esters form following digestion with pancreatic lipase?

A

Cholesterol and 1 free fatty acid.

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47
Q

What happens to phospholipids during digestion with pancreatic lipase?

A

Hydrolysed to lysophospholipids.

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48
Q

What are lysophospholipids?

A

Product of phospholipid hydrolysis during digestion with pancreatic lipase.

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49
Q

What do digested lipids form?

A

Mixed micelles with bile salts.

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50
Q

What are mixed micelles?

A

Aggregates of digested lipids and bile salts following digestion with pancreatic lipase.

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51
Q

How do mixed micelles act?

A

Mixed micelles approach membranes and release lipid products through diffusion.

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52
Q

How do mixed micelles release lipid products at the cell membrane?

A

Diffusion.

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53
Q

What is steatorrhea?

A

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

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54
Q

What can cause steatorrhea?

A

Defects in:
Bile secretion
Pancreatic function
Intestinal cell uptake

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55
Q

What does steatorrhea result in?

A

Excess fat in faeces- stools float due to lipid mass, have an oily appearance and are foul smelling.

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56
Q

How can gallbladder removal affect lipid malabsorption?

A

Gallbladder secretes bile- removal inhibits lipid digestion and absorption of fats which can cause steatorrhea.

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57
Q

What do intestinal cells do?

A

Resynthesise TAG / PL / CE for export.

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58
Q

What resynthesises TAG / PL / CE for export?

A

Intestinal cells.

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59
Q

How do intestinal cells resynthesise TAG/PL/CE for export?

A

Package them with apoB-48 solubilising protein into chylomicrons.

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60
Q

What is apoB-48?

A

Solubilising protein which lipids are packaged with into chylomicrons forming digestion.

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61
Q

What are chylomicrons?

A

Packages of lipids and solubilising protein (apoB-48).

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62
Q

How are chylomicrons released?

A

Released through exocytosis into lymph and then the blood.

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63
Q

What happens to TAG in chylomicrons when they reach tissue?

A

Hydrolysed by lipoprotein lipase into fatty acids and glycerol.

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64
Q

What hydrolyses TAG in chylomicrons when they reach tissue?

A

Lipoprotein lipase.

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65
Q

What reaction occurs between lipoprotein lipase and TAG in chylomicrons when they react tissues?

A

Hydrolysis.

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66
Q

What happens to the fatty acids after they are separated from the chylomicron TAG in tissues?

A

Used for energy or re-esterified to TAG for storage.

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67
Q

What happens to the glycerol after it is separated from the chylomicron TAG in tissues?

A

Used in glycolytic processes.

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68
Q

What happens to chylomicrons depleted of TAG when they reach tissues?

A

Go to the liver as chylomicron remnants.

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69
Q

How does TAG exist in adipose cells?

A

Lipid droplets.

70
Q

How are fatty acids released from stored TAG in adipose cells?

A

Hormone-sensitive lipase is activated by phosphorylation in response to epinephrine which releases FA.

71
Q

What is HSL?

A

Hormone-sensitive lipase.

72
Q

What is HSL activated and inactivated by?

A

Activated by phosphorylation in response to epinephrine which releases the fatty acids from TAG lipid droplets. Increased blood glucose or insulin inhibits the phosphorylation.

73
Q

How are free fatty acids transported in the blood?

A

In complex with serum albumin.

74
Q

What is the most abundant plasma protein?

A

Albumin.

75
Q

What does serum albumin allow and how?

A

Travel of free fatty acids in the blood- has binding sites for them.

76
Q

What happens to most fatty acids?

A

Esterified and travel in lipoproteins (HDL/LDL etc).

77
Q

What are lipoproteins?

A

Proteins with lipid attachments- have hydrophobic cores (TAG/CE) and hydrophilic surfaces (cholesterol, PL).

78
Q

What are lipoproteins classified according to?

A

Density.

79
Q

What is VLDL?

A

TAG from the liver to tissues.

80
Q

What does LDL do?

A

Transports cholesterol to extrahepatic tissues (NOT LIVER)

81
Q

What does HDL do?

A

Transports cholesterol to hepatic tissues (LIVER).

82
Q

Why is HDL good?

A

Removes cholesterol for excretion and prevents excess buildup.

83
Q

Why is LDL bad?

A

Can lead to an increased build-up of cholesterol and subsequent deposition of plaques in blood vessels.

84
Q

What is atherosclerosis?

A

Atherosclerosis is the formation of plaques on vascular arteries- these can build up and result in clots and embolism which have high cardiovascular risks.

85
Q

What process is used to oxidise fatty acids as fuels?

A

Beta-oxidation.

86
Q

What is beta-oxidation?

A

The process used to oxidise fatty acids as fuel molecules.

87
Q

How does beta-oxidation work?

A

Degrades fatty acids 2C at a time- produces energy sources.

88
Q

In what structure does beta-oxidation degrade fatty acid molecules?

A

Degrades them 2C at a time.

89
Q

What does beta-oxidation produce?

A

Acetyl CoA

NADH/FADH2

90
Q

Where does beta-oxidation occur?

A

Mitochondrial matrix.

91
Q

What are the 3 stages of beta-oxidation?

A

Activation of fatty acids
Transport into mitochondria
Degradation into energy sources

92
Q

What can the products of beta-oxidation be used in?

A

Energy production.

93
Q

What happens in the first stage of beta-oxidation?

A

Fatty acids are activated to form fatty acyl CoA in the cytoplasm.

94
Q

Where does fatty acid activation occur?

A

Cytosol.

95
Q

What do activated fatty acids form?

A

Fatty acyl CoA.

96
Q

Where do activated fatty acids need to be for beta-oxidation to occur?

A

Mitochondrial matrix.

97
Q

How do short and medium chain fatty acids reach the mitochondrial matrix for beta-oxidation?

A

Diffuse freely.

98
Q

How do long chain fatty acids reach the mitochondrial matrix reach the mitochondrial matrix for beta-oxidation?

A

Carnitine shuttle.

99
Q

What is the carnitine shuttle?

A

A shuttle used to let activated fatty acids in the cytosol reach the mitochondrial matrix for beta-oxidation.

100
Q

How does the carnitine shuttle work?

A

CPT1 exchanges carnitine for the CoA group to form a conjugate which can be transported through the matrix. In the matrix, CPT2 exchanges CoA for the carnitine group to produce fatty acyl CoA again, ready for oxidation.

101
Q

What molecules exchange carnitine for CoA groups?

A

CPTI, CPTII

102
Q

What does the FA enter the matrix as?

A

Fatty acid conjugate with carnitine.

103
Q

How is the FA conjugate transported into the matrix?

A

Transporter protein.

104
Q

What happens to free carnitine in the matrix?

A

It is shuttled back out in order to maintain free cytoplasmic supply and allow the process to continue as required.

105
Q

What is the carnitine shuttle regulated by?

A

Malonyl CoA.

106
Q

How does malonyl CoA regulate the carnitine shuttle?

A

Has ability to inhibit the process to prevent simultaneous synthesis and degradation.

107
Q

Why might malonyl CoA inhibit the carnitine shuttle?

A

To prevent simultaneous synthesis and degradation.

108
Q

How is carnitine obtained in the body?

A

Found in diet- can also be produced by the liver and kidneys.

109
Q

What do carnitine deficiencies lead to?

A

No beta-oxidation happening- leads to hypoglycaemia.

110
Q

How is carnitine-deficient linked hypoglycaemia treated?

A

Administration of intravenous glucose or a short/medium chain fatty acid that doesn’t need carnitine shuttle.

111
Q

What are the 4 steps of beta-oxidation degradation?

A

Dehydrogenation- produces FADH2
Hydration
Dehydrogenation- produces NADH
Thiolysis- cleaved to produce acetyl CoA

112
Q

What happens in the first dehydrogenation within degradation?

A

Production of FADH2.

113
Q

What happens in the second dehydrogenation within degradation?

A

Production of NADH.

114
Q

What happens in the thiolysis stage of degradation in beta-oxidation?

A

Cleavage to produce acetyl CoA.

115
Q

What does each cycle of beta-oxidation produce?

A

1 Acetyl CoA
A species 2C shorter than the original
129 ATP

116
Q

How much ATP does beta-oxidation yield?

A

129ATP

117
Q

Why are fatty acids more efficient fuels than glucose?

A

Production of 129 ATP compared to 2/32 ATP.

118
Q

What happens to very long chain fatty acids in excess of 22C?

A

Preliminary oxidation in the peroxisome- they are then transported to the mitochondrial matrix.

119
Q

Where does preliminary oxidation of very long chain fatty acids occur? (>22C)

A

Peroxisome.

120
Q

Why is preliminary oxidation in the peroxisome less efficient than normal beta-oxidation?

A

First step doesn’t produce FADH2.

121
Q

What happens to preliminary oxidised fatty acids?

A

Transported to the mitochondrial matrix for normal beta-oxidation.

122
Q

What do defects in the preliminary oxidation pathway result in?

A

Build-up of long chain fatty acids in the bloodstream.

123
Q

Can fatty acids by converted to glucose?

A

No- they are not gluconeogenetic because of the thermodynamically irreversible step converting pyruvate to acetyl CoA.

124
Q

Why are fatty acids non-gluconeogenetic?

A

Cannot bypass the thermodynamically irreversible step converting pyruvate to acetyl CoA.

125
Q

When is the liver flooded with excess acetyl CoA from fatty acid breakdown?

A

During fasting or starvation.

126
Q

What can excess acetyl CoA be converted into?

A

Ketone bodies.

127
Q

What are ketone bodies?

A

Water-soluble transporters of acetyl CoA.

128
Q

What is the process of acetyl CoA conversion into ketone bodies called?

A

Ketonegenesis.

129
Q

Why are ketone bodies good?

A

They can be utilised as an energy source.

130
Q

When is the use of ketone bodies as an energy source particularly useful?

A

In systems that cannot use fatty acids as an energy source (e.g. cardiac/brain/skeletal muscle).

131
Q

Where are ketone bodies formed?

A

Liver matrix.

132
Q

Where do ketone bodies go after formation in the liver?

A

Transported in the blood to tissues as required as they are soluble.

133
Q

What is the rate of ketonegenesis dependent on?

A

The free availability of acetyl CoA.

134
Q

Can the liver use ketone bodies?

A

No- it can make them but not use them.

135
Q

Why is excessive ketonegenesis bad?

A

Can cause a range of clinical issues due to induced ketoacidosis.

136
Q

What diagnostics show excessive ketonegenesis?

A

Ketonaemia (blood KB)
Keonuria (blood urine)
Acidemia

137
Q

What are excessive ketone bodies characterised by?

A

Fruity odour in the breath.

138
Q

What are ketone bodies a breakdown product of?

A

Acetone.

139
Q

What does acetone cause?

A

Distinguishing fruity odour in the breath.

140
Q

In what conditions is excessive ketonegenesis often seen?

A

Uncontrolled diabetes

Starvation

141
Q

How are fatty acids obtained in the body?

A

Essential fatty acids in diet

Synthesis in body

142
Q

Where are fatty acids synthesised?

A

Liver
Lactating mammary gland
Adipose tissue

143
Q

What does fatty acid synthesis require?

A

Acetyl CoA
NADPH
ATP

144
Q

Where in the cell does fatty acid synthesis occur?

A

Cytosol.

145
Q

Where must acetyl CoA be for fatty acid synthesis?

A

Cytosol- must be transported from the mitochondrial matrix following glycolytic production.

146
Q

What transports acetyl CoA from the mitochondrial matrix to the cytosol for fatty acid synthesis?

A

Citrate shuttle.

147
Q

What activates the citrate shuttle?

A

High mitochondrial citrate concentration.

148
Q

What enzymes are involved in fatty acid synthesis?

A

Acetyl CoA carboxylase

Fatty acid synthase

149
Q

What is the product of fatty acid synthesis?

A

Palmitate.

150
Q

What is the first reaction in fatty acid synthesis?

A

Acetyl CoA > Malonyl CoA

151
Q

What is acetyl CoA to malonyl CoA catalysed by?

A

Acetyl CoA carboxylase.

152
Q

What does acetyl CoA carboxylase catalyse?

A

Conversion of acetyl CoA to malonyl CoA.

153
Q

What is acetyl CoA carboxylase activity controlled by?

A

ACC.

154
Q

How does ACC control work?

A

Activated by citrate
Deactivated by palmitoyl CoA
Activated by insulin, deactivated by epinephrine/glucagon

155
Q

How does fatty acid synthesis occur after the conversion of acetyl CoA to malonyl CoA?

A

Multistep process with a multi-functioning enzyme.

156
Q

What is the general reaction for fatty acid synthesis?

A

Acetyl CoA + Malonyl CoA > Palmitate

157
Q

How many NADPH are required for palmitate synthesis?

A

14.

158
Q

Where does the NADPH come from in fatty acid synthesis?

A

Derived from the pentose-phosphate pathway.

159
Q

What does the synthesis of palmitate use up?

A

Carbon dioxide.

160
Q

Where does any further modification of palmitate or dietary fatty acids occur?

A

Mitochondria / ER with diverse range of enzymes.

161
Q

Can fatty acid synthesis and degradation occur at the same time?

A

No.

162
Q

What are steroid hormones?

A

Chemicals that serve as messengers.

163
Q

What are steroid hormones characterised by?

A

Steroid ring.

164
Q

What is cholesterol?

A

Cell membrane component.

165
Q

Where is cholesterol synthesised?

A

Liver- dietary meats.

166
Q

What drug is cholesterol controlled by?

A

Statins.

167
Q

What are eicosanoids?

A

Signalling molecules derived from 20C eicosanoid acids.

168
Q

What are eicosanoids the precursor for?

A

Prostaglandins
Thromboxanes
Leukotrienes

169
Q

What do prostaglandins link with?

A

Link with pain and fever.

170
Q

What do thromboxjnes link with?

A

Blood clotting pathways.

171
Q

What do leukotrienes link with?

A

Bronchioconstriction / smooth muscle contraction.

Science for Medicine (19 decks)

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