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Biochem Final > Lipids > Flashcards

Lipids Flashcards

1
Q

energy storage, biological membranes, protein modification, signal transduction, and digestion of food

A

functions of lipids

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2
Q
  • one polar end (carboxyl group) and a long hydrophobic tail (alkyl chain)
  • humans usually have an even number of carbons (16-20)
A

structure of fatty acid

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3
Q
  • 3 FAs esterfied to a glycerol

- very hydrophobic

A

triacylglyerol (TAG)

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4
Q

location of FA synthesis

A

cytoplasm

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5
Q

location of FA degradation

A

mitochondria

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6
Q

Human FA desaturases can only introduce double bonds where?

A

proximal half (up to carbon 9)

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7
Q

Essential FAs

A 
Linoleic acid (omega 6)>>arachidonic acid
Linolenic acid (omega 3)
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8
Q

Can TAG be transported?

A

No, it’s too hydrophobic. It must be broken down to FFAs first

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9
Q

What is the regulated step of FA degradation?

A

Carnitine-palmitoyltransferase I (CPT1)

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10
Q

Where does FA degradation occur?

A

mitochondria

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11
Q

What does FA break down to?

A

acetyl-CoA

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12
Q

produces CO2 and shortens FA chain by one carbon

A

alpha-oxidation

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13
Q

produces acetyl-CoA (2C’s)

A

beta-oxidation

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14
Q

ketone is made from…

A

acetyl-CoA

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15
Q

What reducing equivalents are made during FA degradation?

A

FADH2 and NADH

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16
Q

How is the degradation of unsaturated FA differ than that of saturated FA?

A

requires isomerases to move the double bonds until it looks like simple FA, then proceeds the same way via beta-oxidation

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17
Q

beta-oxidation in peroxisomes

A

occur in liver and kidney
minor fraction of FAs are degraded this way.
- H2O2 instead of FADH2
- degrades long chains down to 8 C’s

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18
Q

hypoglycemia with unusually low level of ketones in blood and urine

A

FA degradation disorder because it interferes with production of ketone bodies

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19
Q

Acute Fatty Liver of Pregnancy

A

long-chain hydroxyacyl-CoA dehydrogenase deficiency leading to accumulation of long chain FAs in liver. rare condition that can occur in pregnant women in the third trimester.

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20
Q

Non-ketotic Hypoglycemia

A
  • FA import disorder (carnitine deficiency)

- Acyl-CoA Dehydrogenase Deficiencies (along with accumulation of FAs)

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21
Q

problems with alpha-oxidation of phytanic acid (branched-FA). patient presents with accumulation of phytanic acid in blood and tissues, also neurological defects

A

Refsum Disease

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22
Q

accumulation of long FAs (24-26Cs), plasmologen deficiency, myelination deficiency

A

Zellweger Syndrome - dysfunctional peroxisomes

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23
Q

In what organs does synthesis of ketone bodies occur?

A

liver and kidney

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24
Q

What is the regulated step in synthesis of ketone bodies?

A

HMG-CoA lyase

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25
Q

What intermediate of ketone body synthesis can also be part of cholesterol synthesis?

A

acetoacetyl-CoA

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26
Q

What enzyme is used by both synthesis of ketone bodies and cholesterol?

A

HMG-CoA synthase

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27
Q

What can’t the liver and kidney break down ketone bodies?

A

missing aceoacetate/succinyl-CoA transferase (catalyzes HMG-CoA»acetoacetyl-CoA)

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28
Q

How many molecules of acetyl-CoA does it take to make a ketone body?

A

two

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29
Q

high ketone concentrations

A

metabolic acidosis

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30
Q

What types of FAs are gluconeogenic?

A

odd number FAs: break down to 1 acetyl-CoA and 1 propinoyl-CoA (gluconeogenic)

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31
Q

How does acetyl-CoA get transported out to mitochondria?

A

citrate cleavage pathway

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32
Q

ATP-citrate lyase

A

citrate»acetyl-CoA+OAA using one ATP

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33
Q

What does high level of cytoplasmic citrate indicate?

A

CAC is not able to keep up with all the acetyl-CoA. Glycolysis slows and FA synthesis increases

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34
Q

In the reaction catalyzed by malic enzyme (malate»pyruvate), what else is produced?

A

NADPH

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35
Q

Regulated step of FA synthesis

A

Acetyl-CoA» Malonyl-CoA catalyzed by acetyl-CoA carboxylase

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36
Q

Where does FA synthesis occur in a cell?

A

cytosol

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37
Q

large multifunctional enzyme that catalyzes the synthesis of 16 carbon FA (palmitic acid) without releasing an intermediate

A

FA synthase

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38
Q

Both synthesis and elongation of FAs occur at which end of the molecule?

A

carboxyl-end

not omega end

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39
Q

Where in the cell does elongation of FAs occur?

A

either mitochondria or ER

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40
Q

In the ER, what is the carbon donor for elongation of FA?

A

malonyl-CoA (located outside the mitochondrial)

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41
Q

In the mitochondria, what is the carbon donor for elongation of FA?

A

acetyl-CoA (located inside the mitochondria)

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42
Q

Both elongation and desaturation of FA requires what?

A

NADPH

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43
Q

What does desaturation occur in the cell?

A

ER

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44
Q

Desaturation of FA uses what system?

A

p450 monoxygenase system

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45
Q

What does TAG synthesis require from glycolysis during well-fed state?

A

glycerol donor:

DHAP»Glycerol-3-Phosphate catalyzed by glycerol phosphate dehydrogenase

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46
Q

What is the committed step of TAG synthesis?

A

catalyzed by DGAT (acyl-CoA:diacylglycerol acyltransferases)

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47
Q

In the reverse of TAG synthesis (hydrolysis of TAG), what is the enzyme that catalyzes the reaction?

A

lipases

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48
Q

What does hydrolysis of TAG yield?

A

TAG+3H20»Glycerol+3FA

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49
Q

What induces the expression of acetyl-CoA carboxylase, FA synthase, malic enzyme and G6PD?

A

insulin

50
Q

What do malic enzyme and G6PD have in common?

A

they both produce NADPH (important for FA synthesis)

51
Q

What allosterically activate acetyl-CoA carboxylase and FA synthase?

A

citrate

52
Q

The presence of malonyl-CoA inhibits what?

A

FA degradation

53
Q

protein coat surrounding fat droplets

A

perilipin

54
Q

hormone-sensitive lipase is active under what hormone?

A

glucagon

55
Q

What transports FFAs in the circulation?

A

albumin

56
Q

Why does TAG synthesis also occur during fasting state?

A

too much FFAs are released so the liver re-esterifies them back to TAG

57
Q

synthesis of membrane lipids begins with the formation of …

A

diacylglycerol (DAG) from lgycerol phosphate and acyl-CoA

58
Q

What enzyme catalyzes the rate-limiting step in the synthesis of phosphotidylcholine?

A

phosphocholine cytidyltransferase

59
Q

What are the general reactions to membrane lipid synthesis (PC & PE)?

A

X is either choline or ethanolamine

1) activation by phosphorylation
2) transfer to CTP to make CDP-X
3) X transferred from CDP-X to DAG to make phosphotidyl-X

60
Q

What enzyme is involved in the synthesis of phosphotidylserine? What reaction does it catalyze?

A

phosphotidylserine synthase

- exchanges ethanolamine from PE with serine

61
Q

What enzyme is involved with the synthesis of phosphotidylinositol? What reaction does it catalyze?

A

phosphotidylinositol synthase

- CDP-DAG binds with inositol

62
Q

How does the synthesis of PI differ than the synthesis of PE or PC?

A

CTP binds with DAG first, not the head group

63
Q

helps with folding of mitochondrial ETS and buffers electrons in membranes

A

cardiolipin

64
Q

outer leaflet membrane lipids

A

phosphotidylcholine (PC) and sphingomyelin

65
Q

inner leaflet membrane lipids

A

phosphotidylethanolamine (PE)

phosphotidylserine (PS)

66
Q

the transfer of this membrane lipid to the outer leaflet signals apoptosis

A

PS (phosphotidylserine)

67
Q

functions to exchange FAs on membrane lipids

A

phospholipases

  • phospholipase A1»C1
  • phospholipase A2»C2
  • phospholipase C»removes phosphate head from C3
68
Q

What important signal transduction reaction does phospholipase C catalyzes?

A

PIP2»IP3+DAG

69
Q

Which phospholipase produces the signaling molecules prostaglandin and thromboxane?

A

phospholipase A2

70
Q

What essential acid is required for the synthesis of arachidonic acid?

A

Linoleic Acid

71
Q

What are the steps to the synthesis of arachidonic acid?

A

1) elongation and desaturation of linoleic acid to make arachidonic acid
2) it gets incorporated into the phospholipid membrane until signal
3) upon stimulation, phospholipase A2 cleaves arachidonic acid from C2

72
Q

What is the substrate in the synthesis of prostaglandins?

A

free arachidonic acid

73
Q

What enzyme is involved with the synthesis of prostaglandins?

A

COX1/2 and Prostaglandin synthase

74
Q

What enzyme is involved with the synthesis of thromboxanes?

A

thromboxane synthase

75
Q

What enzyme is involved with the synthesis of leukotrienes?

A

lipoxygenase reaction

76
Q

What can potentially inhibit the synthesis of leukotrienes?

A

corticosteroids (inhibits phospholipase A2)

lipoxygenase inhibitors

77
Q

What can potentially inhibit the synthesis of prostaglandins?

A

corticosteroids (inhibits phospholipase A2)

aspirin or NSAIDs (inhibits COX1/2 and prostaglandin synthase)

78
Q

cannot be stored and readily diffuses across membrane

A

prostaglandins

79
Q

promotes smooth muscle contraction, involved with anahylaxis, asthma can be alleviated with the enzyme inhibitor

A

leukotrienes, lipoxygenase inhibitors

80
Q

inflammatory processes - causes vasodilation
during delivery- contraction of uterus
blood - inhibits platelet aggregation

A

prostaglandins

81
Q

condensation of leukotriene A4 with glutathione makes…

A

leukotriene C4

82
Q

membrane lipid with fatty alcohol in ether-linkage

A

plasmalogens

83
Q

induction of ether linkage in the synthesis of plasmalogens must occur where?

A

peroxisomes

84
Q

1 FA, 1 polar head group on sphingosine (no glycerol)

A

sphingolipid

85
Q

ceramide + phosphocholine

A

sphingomyelin

86
Q

ceramide + glucose or galactose

A

cerebrosides

87
Q

cerebrosides + sulfate group

A

sulfatide

88
Q

ceramide + 2-4 neutral sugars

A

globosides

89
Q

ceramide + negative charged NANA (N-acetyl neuraminic acid)

A

gangliosides

90
Q

glycosphingolipids are found…

A

on the outside of the cell because they are glycosylated

91
Q

genetic defects in any of the enzymes required to break down glycolipids will lead to accumulation of undegraded glycolipids in the lysosomes of phagocytic cells

A

sphingolipidoses

92
Q

defect in the enzyme beta-glucosidase leading to accumulation of glucocerebroside, symptoms include liver and spleen enlargement, erosion of long bones

A

Gaucher Disease

93
Q

defect in the enzyme beta-hexosaminidase A leading to accumulation of ganglioside GM2, symptoms include intellectual disability, blindness, cherry red spot on macula, death before age 3

A

Tay-Sachs Disease

94
Q

Where does the synthesis of cholesterol occur (organs)?

A

liver, intestines, and reproductive tissues

95
Q

What cell compartment does the synthesis of cholesterol occur?

A

cytosol

96
Q

What is the rate-limiting step for the synthesis of cholesterol?

A

HMG-CoA reductase (HMG-CoA»Mevalonic Acid), takes 2 NADPH

97
Q
  • can be converted to dolichol-P
  • used in prenylation of proteins
  • precursor for synthesis of CoQ
A

Farnesyl PP

98
Q

Regarding regulation of HMG CoA Reductase, what does the action of phosphorylation by AMP-dependent kinase do?

A

inactivates cholesterol synthesis

99
Q

Regarding regulation of HMG CoA Reductase, what does insulin-dependent dephosphorylation do?

A

activates it thus cholesterol synthesis occurs when blood glucose increases

100
Q

Regarding regulation of HMG CoA Reductase, what does the presence of cholesterol do?

A

end-product inhibition

101
Q

hydrophilic surface and lipophilic core

A

lipoproteins

102
Q

What enzyme catalyzes the esterification of cholesterol to make cholesteryl ester?

A

LCAT (lecitin:cholesterol acyltransferase)

103
Q

found in hydrophobic center of lipoproteins or in cytoplasmic fat droplets

A

cholesteryl esters

104
Q

Regarding the regulation of hormone-sensitive lipase (HSL), what does insulin do?

A

inhibits HSL - prevents release of FFA during well-fed state

105
Q

Regarding the regulation of hormone-sensitive lipase (HSL), what does cortisol do?

A

induces HSL - increases release of FFA from adipose tissue

106
Q

Regarding the regulation of hormone-sensitive lipase (HSL), what does glucagon do?

A

stimulates HSL and it’s mediated by cAMP and PKA

107
Q
  • acidic and water-soluble
  • secreted by the liver through the bile duct into the digestive tract and are very effective in emulsifying fat from the diet
A

bile acids

108
Q

cannot be degraded by human enzymes, must be excreted in the form of bile acids

A

cholesterol and its derivatives

109
Q
  • regulates entry
  • activator of LCAT
  • extract lipids from membranes
A

ApoA

110
Q

structural proteins that give lipoproteins its structures

A

ApoB

ApoB100 - VLDL, ApoB48 - chylomicrons

111
Q
  • regulates the exit

- modulates function of lipoprotein lipase (LPL)

A

ApoC

112
Q
  • marks the surface to help mediate interactions with receptors
  • removal of remnant particles
A

ApoE

113
Q

secreted into the lymphatic system and enter blood through thoracic duct

A

chylomicrons

114
Q

packed with TAGs synthesized by enterocytes from dietary fats

A

chylomicrons

115
Q

functions to distribute dietary lipids throughout the body

A

chylomicrons

116
Q

How do chylomicron remnants get removed?

A
  • by the liver
  • ApoB48 and ApoE on the remnants bind to LDL receptors on the surface of hepatocytes. This initiates receptor-mediated (clarthrin) endocytosis
117
Q

function in reverse cholesterol transport from the peripheral tissues to the liver

A

HDL

118
Q

delivers lipids made by the liver to peripheral tissues

A

VLDL

- leaves full and drop things off

119
Q

leaves the liver empty and brings back cholesterol picked up from peripheral tissues

A

HDL (reverse cholesterol transport)

120
Q

enzyme that transports cholesterol actively out of the cell membranes to HDL

A

ATP-binding Transporter A1 (ABCA-1 aka Cholesterol Efflux Regulatory Protein (CERP))

121
Q

enzyme that esterfies cholesterol once it has been transferred into HDL

A

LCAT (lecitin:cholesterol acyltransferase)

122
Q

liberates FFAs and glycerol from TAGs within the lipoproteins

A

lipoprotein lipase (LPL)

Biochem Final (21 decks)

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