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ANS 328 I: Principles of Nutrition > Lipids > Flashcards

Lipids Flashcards

1
Q

What are the 4 types of dietary lipids?

A
  1. Triacylglycerols (TAGs).
  2. Phospholipids (PLs).
  3. Cholesterol and cholesteryl esters (CEs).
  4. Fat-soluble vitamins (FSVs).
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2
Q

What are the components of a TAG?

A

Glycerol and 3 Fatty acid tails.

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3
Q

What are the 4 FSVs?

A

A, D, E, K.

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4
Q

What are the components of a CE?

A

Cholesterol + FA.
*Dietary form of cholesterol.

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5
Q

Where are phospholipids found in the diet?

A

Everything that has cells.

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6
Q

Where does lipid digestion begin?

A

In the stomach.

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7
Q

What enzyme starts lipid digestion in the stomach?

A

Gastric lipase.

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8
Q

How does gastric lipase begin lipid digestion?

A

It removes 1 FA from the TAGs on the outside of the “clump” of fat, forming diacylglycerols (DAGs).
*Does not get to all TAGs.

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9
Q

What happens when chyme enters the small intestine (SI)?

A

Cholecystokinin (CCK) is released.

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10
Q

What does CCK cause to occur?

A
  1. It causes the pancreas to release pancreatic lipase and pancreatic colipase.
  2. It causes the gallbladder to release bile*.
    *Except for horses, where the liver consistently secretes small amounts of bile directly into the SI, due to lacking a gallbladder.
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11
Q

What effect does bile have on lipids?

A

Surrounds the lipids and breaks them into smaller pieces, called emulsified droplets.

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12
Q

What are emulsified droplets?

A

Droplets that have a lipid in the center and bile acids/salts around the outside, allowing the emulsified droplets to move through the aqueous environment of the SI.

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13
Q

What effect does pancreatic colipase have on lipids?

A

Binds to emulsified droplets and allows pancreatic lipase to access the lipids in the emulsification droplets.

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14
Q

What effect does pancreatic lipase have on lipids?

A

Removes 2 FAs from TAGs and 1 FA from DAGs to form monoacylglycerols (MAGs).

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15
Q

What are the products of lipid digestion?

A

MAGs and FAs.

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16
Q

What are emulsified droplets referred to as during lipid absorption?

A

Mixed bile salt micelles.

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17
Q

Where are MAGs and FAs absorbed?

A

At the brush border, where many transporters move them into epithelial cells.

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18
Q

What transports MAGs and FAs after absorption?

A

Fatty acid binding proteins (FABP).

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19
Q

Where are the MAGs and FAs transported to after being absorbed at the brush border?

A

To the endoplasmic reticulum.

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20
Q

What two events happen in the endoplasmic reticulum?

A
  1. Reesterification of TAGs.
  2. Packaging into chylomicrons.
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21
Q

What are chylomicrons?

A

Lipid transporters that contain all lipid components.

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22
Q

What system do chylomicrons enter after leaving the endoplasmic reticulum?

A

The lymphatic system, which returns fluid (and chylomicrons) to the bloodstream at the vena cava.

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23
Q

How does lipid digestion occur in ruminants?

A

A TAG is separated into glycerol and 3 fatty acids.

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24
Q

What happens to glycerol in the rumen?

A

The glycerol is converted into a VFA, which is absorbed through the rumen wall.

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25
Q

What happens to fatty acids in the rumen?

A

They are turned into polyunsaturated fatty acids (PUFAs) and then undergo biohydrogenation (which removes double bonds) to form saturated fatty acids (SFAs) because PUFAs are toxic to microbes.

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26
Q

What are the end products of lipid digestion in the rumen?

A

VFAs and SFAs.

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27
Q

What are the 4 types of lipoproteins?

A
  1. Chylomicrons.
  2. Very low density lipids (VLDL).
  3. Low density lipids (LDL).
  4. High density lipids (HDL).
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28
Q

What does the density of the lipid refer to?

A

The ratio of protein to lipid. The more protein, the higher the density. Vice versa.

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29
Q

What are apolipoproteins?

A

Proteins associated with lipoproteins that have structural, ligand for receptors, or enzyme cofactor function(s).

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30
Q

How many functions can a apolipoprotein have?

A

1-2.

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31
Q

What function(s) does the apolipoprotein apo CII have?

A

Enzyme cofactor.

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32
Q

What function(s) does the apolipoprotein apo E have?

A
  1. Enzyme cofactor.
  2. Structural.
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33
Q

What function(s) does the apolipoprotein apo B100 have?

A
  1. Ligand for receptors.
  2. Structural.
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34
Q

What is step 1 of chylomicron transport?

A

Chylomicrons are synthesized in the small intestine.

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35
Q

What is step 2 of chylomicron transport?

A

Chylomicrons enter the lymphatic system and are transported into the bloodstream at the vena cava.

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36
Q

What is step 3 of chylomicron transport?

A

Chylomicrons associate with apo CII in the blood, which binds to lipoprotein lipase on capillary walls.

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37
Q

What is step 4 of chylomicron transport?

A

Lipoprotein lipase causes TAGS to be broken into glycerol and FAs.

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38
Q

What is step 5 of chylomicron transport?

A
  1. Glycerol goes to the liver.
  2. FAs go to nearby tissues for energy and storage.
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39
Q

What is step 6 of chylomicron transport?

A

The chylomicrons continue to circulate until 80% of the TAGs are released.

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40
Q

What is step 7 of chylomicron transport?

A

Apo CII disassociates from the chylomicron and the chylomicron becomes a chylomicron remnant.

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41
Q

What is step 8 of chylomicron transport?

A

The chylomicron remnant is removed from the bloodstream when apo B48 binds to receptors on liver cells.

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42
Q

When is chylomicron synthesis occurring?

A

Fed state.

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43
Q

What is step 1 of VLDL transport?

A

VLDLs enter the bloodstream and associates with apo CII.

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44
Q

What is step 2 of VLDL transport?

A

Apo CII binds to lipoprotein lipase on the capillary walls.

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45
Q

What is step 3 of VLDL transport?

A

TAG is broken into glycerol and FAs by lipoprotein lipase.

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46
Q

What is step 4 of VLDL transport?

A
  1. Glycerol goes to the liver.
  2. FAs go into nearby tissues for energy and storage.
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47
Q

What is step 5 of VLDL transport?

A

VLDL continues to circulate in the blood until roughly 50% of the TAGs have been released. Apo CII dissociates and VLDL becomes intermediate density liquids (IDL).

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48
Q

What is step 6 of VLDL transport?

A

IDL circulates and releases TAGS through apo E receptors on the capillary walls.

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49
Q

What is step 7 of VLDL transport?

A

Once another roughly 30% of the TAGs are released, apo E dissociates and IDL becomes LDL.

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50
Q

When does VLDL transport occur?

A

When fat is synthesized in the liver and transported to other tissues in the body.

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51
Q

What apolipoproteins do VLDLs have?

A
  1. Apo B100.
  2. Apo E.
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52
Q

What is step 1 of LDL transport?

A

Travels through the bloodstream for 2-3 days.

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53
Q

What is step 2 of LDL transport?

A

LDL encounters apo B100 receptors and cholesterol diffuses out of LDL into tissue.

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54
Q

What is step 3 of LDL transport?

A

Once most of the cholesterol in the LDL has been removed, the LDL is removed from circulation via apo B100 receptors on the liver.

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55
Q

When does LDL transport occur?

A

When cholesterol needs to be transported from the liver to other tissues.
*Secondary way to form LDL.

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56
Q

What apolipoprotein is associated with LDL?

A

Apo B100.

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57
Q

What is step 1 of HDL transport?

A

HDL is released from the liver and travels through the bloodstream.

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58
Q

What is step 2 of HDL transport?

A

HDL binds Apo AI receptors on the capillary walls, resulting in the desorption of cholesterol from tissues.

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59
Q

What is step 3 of HDL transport?

A

HDL returns to the liver with cholesterol via apo AI receptors.

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60
Q

When does HDL transport occur?

A

Transporting cholesterol from peripheral tissue to the liver.

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61
Q

What apolipoprotein does HDL have?

A

Apo AI.

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62
Q

What are the 4 biological roles of lipids?

A
  1. Structural components of membranes (ex: phospholipids).
  2. Energy source.
  3. Lubricants (ex: sebaceous gland secretions).
  4. Signaling molecules (ex: Steroid hormones).
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63
Q

What 3 locations in the body does fatty acid synthesis occur in?

A
  1. Adipose tissue (store).
  2. Liver (sent out).
  3. Lactating mammary glands (milk fat).
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64
Q

Where is acetyl-CoA found?

A

Mitochondria.

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65
Q

What enzyme is required to convert pyruvate into acetyl-CoA?

A

Pyruvate dehydrogenase.

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66
Q

What cofactors are required to convert pyruvate into acetyl-CoA?

A

CoA and NAD+ go in, CO2 and NADH+H^+ come out.

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67
Q

What enzyme is required to convert acetyl-CoA and oxaloacetate into citrate?

A

Citrate synthase.

68
Q

What cofactor is required to convert acetyl-CoA and oxaloacetate into citrate?

A

H2O goes in, CoA comes out.

69
Q

What enzyme is required to convert citrate into isocitrate?

A

Aconitase.

70
Q

What enzyme is required to convert isocitrate into alpha-ketoglutarate?

A

Isocitrate dehydrogenase.

71
Q

What are the cofactors required to convert isocitrate into alpha-ketoglutarate?

A

NAD+ goes in, NADH + H^+ and CO2 come out.

72
Q

What would prevent isocitrate from being converted into alpha-ketoglutarate?

A

The ratio of NADH + H^+ : NAD+ being too high.

73
Q

What happens if isocitrate dehydrogenase is inhibited?

A

Aconitase converts isocitrate back into citrate and citrate leaves the mitochondria.

74
Q

What happens as citrate leaves the mitochondria?

A

A malate enters the mitochondria and is converted into oxaloacetate.
*Called the citrate shuttle.

75
Q

What enzyme is required to convert citrate into acetyl-CoA and oxaloacetate?

A

ATP-citrate lyase.

76
Q

What cofactors are required to convert citrate into acetyl-CoA and oxaloacetate?

A

ATP, CoA, and H2O go in, ADP + Pi comes out.

77
Q

What enzyme is required to convert oxaloacetate into malate?

A

Malate dehydrogenase.

78
Q

What cofactor is required to convert oxaloacetate into malate?

A

NAD+ goes in, NADH + H^+ comes out.

79
Q

What enzyme is required to convert acetyl-CoA into malonyl CoA?

A

Acetyl-CoA carboxylase.

80
Q

What activates acetyl-CoA carboxylase?

A
  1. Insulin.
  2. Glucose.
81
Q

What inhibits acetyl-CoA carboxylase?

A

Glucagon.

82
Q

What cofactors are required to convert acetyl-CoA into malonyl CoA?

A

HCO3 and ATP go in, ADP + Pi comes out.

83
Q

Why is the conversion of acetyl-CoA into malonyl CoA important?

A

It is the first committed step of fatty acid synthesis.

84
Q

How much malonyl CoA, acetyl-CoA, and NADPH + H^+ are required to complete fatty acid synthesis?

A

7 malonyl CoA, 1 acetyl-CoA, and 14 (NADPH + H^+).

85
Q

What is required to convert 7 malonyl CoA, 1 acetyl-CoA, and 14 NADPH + H^+ into the final products of fatty acid synthesis?

A

Fatty acid synthase.

86
Q

What are the final products of fatty acid synthesis?

A

Palmitate (16 carbon chain), 8 CoA, 14 NADP+, 7 CO2, and 6 H2O.

87
Q

What are the 2 ways that palmitate is modified?

A
  1. Elongation.
  2. Desaturation.
88
Q

Where does elongation occur?

A

In the ER.

89
Q

How is elongation done?

A

Malonyl CoA donates 2 carbons that are added to the carboxyl end of the palmitate.
*Body always synthesizes even numbered fatty acids.

90
Q

Where do odd numbered FAs in the body come from?

A

The diet.

91
Q

What is the goal of desaturation?

A

To form a monounsaturated fatty acid.

92
Q

Where does desaturation occur?

A

In the ER.

93
Q

Where are the double bonds added during desaturation?

A

At the delta-9, 5, and 6 carbons.
*Delta-9 is always first.

94
Q

How are the double bonds added?

A

Delta-# desaturase.

95
Q

In what direction are the carbons labeled?

A

Starting at the carboxyl group and moving right.

96
Q

What are the types of fatty acids that are found above delta-9?

A

w(omega)-3 or 6 fatty acids.

97
Q

What directions are w-carbons counted in?

A

Starting at the methyl group and moving left.

98
Q

Can w-3 and w-6 fatty acids be synthesized in the body?

A

No, they are primarily found in plants and fish.
*Important in cell signaling.

99
Q

What happens after FAs are produced in the liver and adipose tissue?

A

TAG synthesis.

100
Q

Where does TAG synthesis occur?

A

In the ER.

101
Q

Why does TAG synthesis occur?

A

For the transport and/or storage of fatty acids.

102
Q

What happens if FAs in the liver are not converted into TAGs?

A

A fatty liver.

103
Q

What are TAGs packaged into before leaving the liver?

A

VLDLs.

104
Q

Where are the TAGs absorbed?

A

In extrahepatic tissues.

105
Q

What enzyme facilitates TAG release and storage?

A

Lipoprotein lipase.

106
Q

What enzyme is responsible for TAG mobilization?

A

Hormone sensitive lipase.

107
Q

What hormone inhibits hormone sensitive lipase?

A

Insulin.

108
Q

Where does glycerol go during TAG mobilization?

A

To the liver for gluconeogenesis.

109
Q

Where do FAs go during TAG mobilization?

A

To tissues that need energy.

110
Q

How are FAs transported in the blood?

A

Attached to albumin.

111
Q

When is fatty acid oxidation high?

A

During a starvation state.

112
Q

When is fatty acid oxidation low?

A

During a fed state.

113
Q

What is the rate of FA oxidation proportional to?

A

The concentration of FA in blood plasma.

114
Q

What is the first step of FA transport to the mitochondria?

A

FAs enter the cytosol.

115
Q

What is the second step of FA transport to the mitochondria?

A

A CoA gets attached to form FACoA.

116
Q

What is the third step of FA transport to the mitochondria?

A

The carnitine cycle allows for transport of FACoA from cytosol into mitochondria.

117
Q

What 3 enzymes are involved in the carnitine cycle?

A
  1. Carnitine palmitoyltransferase-I (CPT-I).
  2. Carnitine-palmitoylcarnitine translocase.
  3. Carnitine palmitoyltransferase-II (CPT-II).
118
Q

What is carnitine?

A

An amino acid-like protein that is synthesized from lysine.

119
Q

What is the function of CPT-I?

A

Converts FACoA into FA carnitine in the cytosol.

120
Q

What is the function of carnitine-palmitoylcarnitine translocase?

A

Transports FA carnitine into the mitochondria in exchange for a free carnitine.

121
Q

What is the function of CPT-II?

A

Coverts FA carnitine into FACoA in the mitochondria.

122
Q

What is beta-oxidation?

A

The breakdown of fatty acid to acetyl-CoA in the mitochondria.

123
Q

What is the function of beta-oxidation?

A

To supply energy.

124
Q

What are the reactants for beta-oxidation?

A

Palmitoyl-CoA + 7 CoA + 7 FAD+ + 7 NAD+ + 7 H2O.

125
Q

What are the products for beta-oxidation?

A

8 acetyl-CoA + 7 FADH2 + 7 (NADH + H^+).

126
Q

How much ATP is produced by the oxidation of palmitoyl-CoA to acetyl-CoA?

A

28 ATP.

127
Q

What is the ATP equivalency of acetyl-CoA?

A

10 ATP.

128
Q

How much ATP is produced by the oxidation of acetyl-CoA?

A

80 ATP.

129
Q

What is the total amount of ATP that is produced during beta-oxidation?

A

108 per palmitate.

130
Q

What are ketone bodies?

A

Small byproducts of ketogenesis that are produced as a glucose substitute for the brain and muscle.

131
Q

When are ketone bodies released?

A

During a starvation or fasted state.
*A small amount is consistently produced.

132
Q

Where are ketone bodies released from?

A

Liver.

133
Q

What are the 3 ketone bodies released?

A
  1. Acetone (byproduct that is released).
  2. Acetoacetate (energy).
  3. BHB (energy).
134
Q

What are the levels of ketone bodies in the fed state?

A

10 micro molar.

135
Q

What are the levels of ketone bodies in the fasted state?

A

1 Milimolar.

136
Q

What are the levels of ketone bodies after a 2 day fast?

A

2 Millimolar.

137
Q

Where does ketogenesis occur?

A

Mitochondria.

138
Q

Where is acetone produced from?

A

From acetoacetate. Occurs spontaneously.

139
Q

How is acetoacetate created?

A

Via an enzyme that converts BHB into acetoacetate.
*Reversible.
**Prevents acetone formation.

140
Q

What do ketone bodies become in the mitochondria of muscles and the brain?

A

Acetyl-CoA, which enters the citric acid cycle to produce ATP.

141
Q

What are the 3 stages of ketosis?

A
  1. Ketonemia.
  2. Ketonuria.
  3. Ketoacidosis.
    *Stage stack and become concurrent.
142
Q

What is ketonemia?

A

Elevated levels of ketone bodies in the blood.

143
Q

What is ketonuria?

A

Elevated levels of ketone bodies in the urine, in an attempt to lower the level of ketones bodies in the blood.

144
Q

What is ketoacidosis?

A

A drop in blood pH due to a build up of ketone bodies, as they cannot be excreted fast enough.
*Is followed by death.

145
Q

What is the treatment for ketosis?

A

Glucose bolus, glycerol, propylene glycol.

146
Q

How does excess weight prior to lactation contribute to ketosis?

A

Excess fat is mobilized to form milk fat, instead of having milk fat be synthesized in the mammary glands.

147
Q

Where does cholesterol synthesis occur?

A

In the cytosol of all nucleated cells.

148
Q

What are the major sites of cholesterol synthesis in the body?

A
  1. Liver (VLDLs, LDLs, and HDLs).
  2. Small intestine (chylomicrons).
149
Q

What roles does cholesterol serve in the body?

A
  1. Structural.
  2. Cell signaling.
  3. Steroid hormone synthesis.
150
Q

What purposes are lipids usually used for in a diet?

A
  1. Increase palatability.
  2. Reduce dust.
150
Q

What pathway does the beginning of cholesterol synthesis mimic?

A

Ketone body synthesis.

151
Q

What state of matter is animal fat in at room temperature?

A

Solid.

152
Q

What are the three types of animal fat used in diets?

A
  1. Tallow.
  2. Lard.
  3. Grease.
153
Q

What animals are fed animal fats?

A
  1. Carnivores.
  2. Omnivores.
154
Q

What animals is tallow derived from?

A

Beef and sheep.

155
Q

What animal is lard derived from?

A

Swine.

156
Q

Where is grease obtained?

A

From restaurants.

157
Q

What state of matter are oils in at room temperature?

A

Liquid.

158
Q

What are the oils used in diets?

A
  1. Marine oil.
  2. Vegetable oil.
159
Q

Where is marine oil derived from?

A
  1. Krill.
  2. Fish.
160
Q

Where is vegetable oil derived from?

A

A mixture of vegetables.

161
Q

What is a problem that can arise with fats and oils?

A

Rancidity.

162
Q

What is rancidity?

A

When O2 reacts with bonds between the fatty acids. This leads to an offensive/rancid odor, decreased palatability, and is toxic to animals (build-up of free radicals).

163
Q

What are fats and oils fed with to try and prevent rancidity?

A

Anti-oxidants.

164
Q

What % of the diet do fats and oils make up?

A

3-5%.
*Otherwise, digestive disturbance occurs.

165
Q

What animals can be fed a high lipid (7% lipid) diet?

A
  1. Poultry.
  2. Swine.
166
Q

What animals are less tolerant of dietary fat?

A

Ruminants.

ANS 328 I: Principles of Nutrition (8 decks)

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