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Molecular Block 4 > Block 4 Nishimoto Questions > Flashcards

Block 4 Nishimoto Questions Flashcards

1
Q

Zellweger Syndrome

A

Lack of functional peroxisomes; Can’t Oxidize VLCFA’s

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2
Q

Which steps of Mitochondrial Long-Chain FA Metabolism Occurs in Cytosol?

A

Fatty acyl CoA Synthetase Activates FA to FattyAcylCoA

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3
Q

Which KB packs “extra punch”

A

Beta-hydroxybutyrate (NADH)

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4
Q

Where is Fatty Acyl CoA Oxidized in Liver?

A

Mitochondrial Matrix

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5
Q

Where does Succinyl CoA get its CoA for Ketone Oxidation

A

CAC Cycle or Oxidation of Odd-Chain or Branched-Chain FA’s

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6
Q

Where does Omega-oxidation occur?

A

ER, forms Dicarboxylic Acids

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7
Q

Where does maturation of Chylomicrons occur?

A

Blood, pick up ApoE and ApoCII from HDL

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8
Q

Where does final oxidation of Fatty Acyl CoA occur?

A

Mitochondrial Matrix

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9
Q

Where are OH Groups of Cholesterol in a Lipoprotein

A

Surface

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10
Q

When is MC AcylCoA Dehydrogenase deficiency noticed?

A

When glucose levels are low and FA’s cannot be completely oxidized

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11
Q

When is Gluconeogenesis main source of blood glucose

A

After ~16 hours

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12
Q

When does muscle use blood glucose

A

High insulin (fed state) or during exercise

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13
Q

When does muscle primarly use Glycogen?

A

Severe exersize

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14
Q

When does brain start using KB’s?

A

Roughly day 3 (Starved State); KB levels in blood aren’t high enough until this day.

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15
Q

When do you need extra ATP in Palmitate synthesis?

A

When starting with just Acetyl CoA (no Malonyl CoA)

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16
Q

When are Malonyl CoA levels elevated?

A

Fed State; It’s the substrate for FA Synthesis produced by Acetyl CoA Carboxylase

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17
Q

What size FA’s use Carnitine Cycle for Membrane Transport

A

Long Chain (12-20)

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18
Q

What size FA’s are catabolized in peroxisome?

A

Very Long Chain (>20)

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19
Q

What provides the omega-methyl group of palmitate in FA synthesis?

A

Acetyl CoA

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20
Q

What provides the 2 carbon units that are added to the growing Fatty Acyl chain?

A

Malonyl CoA

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21
Q

What products of lipid digestion do Intestinal epithelial cells absorb?

A

FA’s and 2-MG’s

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22
Q

What percent of Bile Salts are excreted?

A

5

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23
Q

What part of intestinal cell produces TG?

A

sER

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24
Q

What part of intestinal cell produces apoB-48

A

rER

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25
Q

What part of FA Synthase reacts with Malonyl CoA

A

Sulfhydryl group of Phosphopantetheinyl residue

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26
Q

What is required to transfer lipid to apoB-48?

A

MTP

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27
Q

What is required for FA chain to start?

A

An AcCoA is required to be acceptor of Malonyl Transfer; Must make MalonylCoA from AcCoA

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28
Q

What is produced converting Beta-Hydroxybutyrate to Acetoacetate

A

NADH + H+

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29
Q

What is necessary to convert Acetoacetate to Beta-hydroxybutyrate

A

NADH + H+

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30
Q

What is Acetyl CoA from Long-Chain FA Metabolism used for in Liver

A

KB Synthesis (TCA Cycle in other tissues)

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31
Q

What is a key factor in control of Ketone Synthesis

A

Availability of FA’s

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32
Q

What happens to remnants of Chylomicron breakdown?

A

Taken up by liver by receptor-mediated endocytosis; Digested by Lysosomes; Products released into Cytosol

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33
Q

What happens to HMG CoA in Ketone Synthesis

A

Converted to Acetoacetate, producing one AcetylCoA

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34
Q

What happens to FADH2’s produced in VLCFA oxidation?

A

Transfer electrons to O2; Produce H2O2

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35
Q

What happens to FA’s once absorbed into intestinal epithelium?

A

Esterfied to the 2-MG’s to form TG

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36
Q

What happens to Citrate once pumped into Cytosol?

A

Makes OAA and AcCoA

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37
Q

What happens to Bile Salts no longer needed?

A

Absorbed in Ileum, Returned to Liver via Entero-hepatic Circulation

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38
Q

What happens to Acetoacyl CoA in Ketone Oxidation?

A

Cleaved to 2 Acetyl CoA by Thiolase

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39
Q

What happens to 2-MG’s once absorbed into intestinal epithelium?

A

Esterfied to FA’s to form TG’s

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40
Q

What FA’s under Alpha-Oxidation?

A

Branched-Chain FA’s

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41
Q

What enzyme activates Fatty Acids

A

Fatty Acyl CoA Synthetase

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42
Q

What electron carriers are produced during Beta-oxidation?

A

NADH, FADH2

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43
Q

What donates a CoA to Acetoacetate in Ketone Oxidation?

A

Succinyl CoA

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44
Q

What does the Final Step in Oxidation of Odd Chain FA’s produce

A

Propionyl CoA (3 Carbons)

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45
Q

What does the conversion of Proprionyl CoA to Succinyl CoA require?

A

ATP, Biotin, Vitamin B12

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46
Q

What does Pancreatic Lipase require to work?

A

Protein Colipase to stabilize and localize lipase near bile salt-TG particle

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47
Q

What does Pancreatic Lipase Colipase need to work?

A

Bile salts to emulsify TG’s

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48
Q

What does omega-oxidation of FA’s produce?

A

Dicarboxylic Acids -> May be excreted or conjugated to Glycine or Carnitine

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49
Q

What does muscle use during resting state or mild exersize?

A

KBs or FA’s (FA’s preferred)

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50
Q

What does Desaturase require

A

Molecular Oxygen

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51
Q

What does Beta-oxidation of Fatty Acyl CoA generate in mitochondria

A

NADH, FAD(2H), Acetyl CoA

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52
Q

What do Peroxisomes not produce from Beta-Oxidation?

A

FAD(2H)

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53
Q

What bond is cleaved in Beta-oxidation?

A

alpha-beta bond

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54
Q

What activates LPL on capillary walls in adipose and muscle tissue?

A

ApoCII

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55
Q

Uses for FA’s from Adipose during Basal Fasted State

A

Liver for ATP and KB’s (which go to muscle, not brain yet); Muscle for AcCoA/TCA

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56
Q

Types of FA’s oxidized in Peroxisomes

A

VLCFA, Some LCFA’s; Branched-Chain >8

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57
Q

Two products of Glycerol Metabolism in Liver

A

DHP, Glyceraldehyde-3-P

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58
Q

Two Main Ketone Fuels

A

Beta-hydroxybutyrate, Acetoacetate

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59
Q

To what part of FA Synthase is Phosphopantheine linked?

A

Serine residue of Acyl Carrier Protein segment

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60
Q

To what is Alanine from muscle converted?

A

Pyruvate

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61
Q

T/F: the Liver can use KB’s as fuel if is has to

A

False, doesn’t have correct enzymes

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62
Q

T/F: One isozyme of Acyl CoA Dehydrogenase can oxidize all FA lengths?

A

False, several different isozymes

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63
Q

Surface of Lipoproteins

A

Phospholipids and Proteins on surface, with hydrophilic regions interacting w/ water

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64
Q

Subcellular location of FA Activation

A

Cytosol (or Mitochondria???) (Fatty Acyl CoA Synthetase)

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65
Q

Subcellular Location of Elongase

A

Endoplasmic Reticulum

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66
Q

Subcellular Location of Desaturase

A

ER

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67
Q

Subcellular Location of CPT2

A

Inner Mitochondrial Membrane

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68
Q

Subcellular Location of CPT1

A

Outer Mitochondrial Membrane

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69
Q

Steps Unique to VLCFA Oxidation

A

Oxidized in peroxisomes by beta-oxidation to produce medium/short-chain; Converted to Carnitine dervatives and sent to mitochondria

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70
Q

Source of Pyruvate in FA Synthesis

A

Glycolysis (Glucose)

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71
Q

Source of Glycerol for Lipogenesis in Fed State?

A

Glycolysis

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72
Q

Source of Citrate in FA Synthesis

A

Mitchondria: OAA and AcCoA from Pyruvate; AcCoA + OAA = Citrate

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73
Q

Site of Catabolism and Membrane Transport of Very Long Chain FA’s

A

Peroxisome; Unknown

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74
Q

Site of Catabolism and Membrane Transport of Short Chain (2-4) FA’s

A

Mitochondrion; Free Diffusion

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75
Q

Site of Catabolism and Membrane Transport of Medium Chain (4-12) FA’a

A

Mitochondrion; Diffusion

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76
Q

Site of Catabolism and Membrane Transport of Long Chain (12-20) FA’s

A

Mitochondrion; Carnitine Cycle

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77
Q

Role of Fatty Acyl Carnitine

A

Carnatine carries FA into mitochondria (Enzymes required)

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78
Q

Role of CPT1 in Ketone Synthesis Regulation

A

Converts FA’s to FA-Carnitine (which then is converted to FA-CoA)

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79
Q

Role of Citrate in FA Synthesis

A

Provides AcCoA and NADPH for FA Synthesis

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80
Q

Regulation of VLCFA Oxidation

A

Just VLCFA availability

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81
Q

Regulation of Alpha-Oxidation of Branched-Chain FA’s

A

None

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82
Q

Regulated step of FA Synthesis

A

Acetyl CoA converted to Malonyl CoA by AcCoA Carboxylase (Needs CO2, ATP, Biotin)

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83
Q

Reducing agent used by Desaturase

A

NADH

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84
Q

Reducing agent in FA Synthesis vs Beta-Oxidation

A

NADPH vs NADH, FADH2

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85
Q

Recycling of OAA back to mitochondria makes what?

A

NADPH

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86
Q

Pyruvate Carboxylase

A

Pyruvate to OAA

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87
Q

Purpose of Thiolysis in Beta-Oxidation

A

Cleavage step, produces 1 AcetylCoA and FACoA that is 2 carbons shorter

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88
Q

Purpose of Protein Colipase

A

Binds to lipase and emulsified fat increasing lipase action

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89
Q

Products of initial beta-oxidation of VLCFA in peroxisomes?

A

AcetylCoA (Acetyl-Carnitine); SCFA CoA/MCFA CoA (SCFA-carnitine/MCFA-Carnitine)

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90
Q

Products of Beta-Oxidation of Even-Chain FA

A

Acetyl CoA; FADH2, NADH

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91
Q

Production of Dicarboxylic Acids

A

Omega-Oxidation of FA’s; May be excreted or conjugated to Glycine or Carnitine

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92
Q

Processing of Propionyl CoA produced from Odd Chain FA Oxidation

A

Add carbon and form Succinyl CoA

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93
Q

Primary Tissues for FA Synthesis vs Beta-Oxidation

A

Liver, Fat vs Liver, Muscle

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94
Q

Prevention of newly synthesized FA’s from oxidation

A

Malonyl CoA (high during FA synthesis) inhibits CPT1, which tranports LCFAs into mitochondria

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95
Q

Preferred substrate of muscle during prolonged exercise

A

Glucose

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96
Q

Preferred substrate of Cardiac Muscle 2 hours after meal

A

FA

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97
Q

Positive Regulators of Ketogenesis

A

(1) High FA’s; (2) High CPTI; (3) Low Malonyl CoA; (4) High ATP; (5) High NADH; (6) Low OAA

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98
Q

Positive regulation of FA Synthesis

A

Citrate, Insulin

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99
Q

Positive regulation of Acetyl CoA Carboxylase

A

Citrate, Insulin

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100
Q

Net AcetylCoA’s used to make 1 Acetoacetate

A

1 (2 initially, but one produced)

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101
Q

Negative Regulators of Ketogenesis

A

(1) Low FA’s; (2) Low CPTI; (3) High Malonyl CoA; (4) Low ATP; (5) Low NADH; (6) High OAA

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102
Q

Negative regulation of Acetyl CoA Carboxylase

A

Palmitoyl CoA, Low ATP (High AMP)

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103
Q

Negative regulation of Acetyl CoA Carboxylase

A

Palmitoyl CoA, Low ATP (High AMP)

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104
Q

Metabolic Changes when reach Starved State

A

Brain uses KB’s, Muscle doesn’t; Mucles stops breaking down Protein (less Urea in Urine)

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105
Q

Maturation of Chylomicrons

A

Occurs in blood; Pick up ApoE and ApoCII from HDL

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106
Q

Malonyl CoA

A

Inhibits CPT1; When FA’s being synthesized, blocks FA oxidation; Intermediate in FA Synthesis

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107
Q

Malic Enzyme

A

Malate to Pyruvate; Producing CO2 and NADPH

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108
Q

Malate Dehydrogenase

A

OAA to Malate, using NADH

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109
Q

Major target of Glucagon and effect on cAMP

A

Liver, Increases cAMP; (Activates Lipase in Adipose?)

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110
Q

Major Component of a Chylomicron

A

TG

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111
Q

Major apolipoprotein in Chylormicrons

A

apoB-48

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112
Q

Location of HMG CoA Synthase

A

Liver Mitochondria

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113
Q

Lipolytic Hormones

A

Glucagon (fasting, starvation); Epi/NE (stress); ACTH

114
Q

KB levels during prolonged fasting

A

Rise substantially thru day 20-30

115
Q

Intracellular Lipolysis Cascade after Glucagon binds

A

Adenylate Cyclase -> cAMP -> PK -> TAG Lipase -> TAG to DAG to FFA’s -> FFAs released

116
Q

Insulin stimulates the secretion of what from Adipose cells?

A

LPL (Lipoprotein Lipase)

117
Q

Initial Oxidation of Branched-Chain FA’s

A

Alpha-oxidation in Peroxisomes to produce CO2, Propionyl and Acetyl CoA; MCFA’s sent to mitochondria as carnitine derivatives

118
Q

Inhibitor of CPT1

A

Malonyl CoA

119
Q

In what part of intestinal cell does assembly of lipoproteins occur?

A

ER and Golgi

120
Q

In what organ does the synthesis of FA from Glucose mainly occur?

A

Liver

121
Q

In what form are TG’s ultimately absorbed in small intestine?

A

FA’s and 2-MG’s

122
Q

In what form are Hepatic TAG’s exported from Liver

A

VLDL’s

123
Q

In Palmitate Synth., what extra do you need if starting from just AcetylCoA

A

7 ATP to add CO2

124
Q

How many FADH/NADH molecules are produced for each cycle of Beta-oxidation?

A

1 (=4 ATP)

125
Q

How many carbons added with each repeat of FA Synthesis

A

2 Carbons

126
Q

How many ATPs per NADH in FA Oxidation?

A

2.5

127
Q

How many ATPs per FADH2 in FA Oxidation?

A

1.5

128
Q

How many ATPS from 1 Palmitate via Beta-Oxidation?

A

7 Cycles; 7 NADH and 7 FADH2 = 28 ATP; 8 AcCoA = 80; Minus 2 ATP for activation; Total=106 ATP

129
Q

How many ATP are required to Activate Beta-oxidation

A

2

130
Q

How many Acetyl CoA’s does Palmitoyl CoA produce?

A

8, 7 repetitions of the Beta-oxidation spiral

131
Q

How many Acetyl CoA’s are needed to make 1 HMG CoA

A

2

132
Q

How is Acetoacetate activated in Ketone Oxidation?

A

Accepts a CoA group from Succinyl CoA

133
Q

How does Muscle get energy during basal fasted state?

A

KB’s from liver (which come from FA’s from adipose); FA’s directly from Adipose

134
Q

How does low calorie diet affect Acetyl CoA Carboxylase

A

Decreases rate of transcription -> Inhibit FA Synthesis

135
Q

How does Liver get ATP during Basal Fasted State?

A

FA’s from Adipose

136
Q

How does Insulin Ratio induce TG degradation in Adipose?

A

(1) High Glucagon/Insulin elevates cAMP; (2) PKA Activated; (3) Hormone-Sensitive Lipase Phosphorylated; (4) TG broken down into FA and Glycerol

137
Q

How does increased insulin stop TG degradation in Adipose tissue?

A

Stimulates the phosphatase that inactivates HSL in fed state

138
Q

How does high calorie diet affect Acetyl CoA Carboxylase

A

Increases rate of transcription -> Promotes FA Synthesis

139
Q

How does Brain get ATP during Basal Fasted State?

A

Glucose from Gluconeogenesis/Glycogenolysis

140
Q

How do high FA levels affect CPTI

A

Malonyl CoA inhibition of CPTI is lifted by inactivation of AcCoA Carboxylase

141
Q

How do Glucose levels change during Fasting

A

Drop Initially, then remain relatively constant indefinitely

142
Q

How do FFA levels change during fasting

A

Rise initially, then remain relatively constant indefinitely

143
Q

How do fat cells make Glycerol-3-Phosphate

A

From Glucose by Glycolysis; They lake Glycerol Kinase

144
Q

How do activated Acetyl groups exit mitochondria in FA Synthesis?

A

As Citrate

145
Q

How do activate Acyl groups enter mito in Beta-Oxidation

A

As Carnitine Derivative

146
Q

How are the Acetyl CoA’s produced in (terminal step of) Ketone Oxidation

A

Acetoacetyl CoA is cleaved by Thiolase

147
Q

How are dietary FA’s transported in blood?

A

Chylomicrons

148
Q

How are Beta-Oxidation and CAC similar?

A

Hydration, production of FADH2 and NADH

149
Q

Goal of FA Synthesis

A

Store excess glucose as FA’s

150
Q

From what is Acetone spontaneously formed?

A

Acetoacetate, giving off CO2

151
Q

From what does Chylomicron get ApoE and ApoCII

A

HDL

152
Q

From what are Bile Salts derived?

A

Cholesterol (maintain their ring structure)

153
Q

For what does the liver recycle Glycerol?

A

Gluconeogenesis and TG Synthesis

154
Q

First Three Steps of Ketone Synthesis (Just substrates)

A

(1) 2 AcetylCoA –> (2) Acetoacetyl CoA –> (3) HMG CoA

155
Q

First Step of Ketone Oxidation when starting with Beta-Hydroxybutyrate?

A

Oxidation to Acetoacetate

156
Q

First Committed Step of FA Synthesis

A

Acetyl CoA converted to Malonyl CoA by AcCoA Carboxylase (Needs CO2, ATP, Biotin)

157
Q

Fate of Proteins in Muscle during Basal Fasted State

A

Broken down into AA’s, which are used for Gluconeogenesis

158
Q

Fate of FAD(2H) and NADH produced in beta-oxidation of FA’s

A

Re-oxidized by ETC, producing ATP

159
Q

Extra requirements of Beta-Oxidation of Unsaturated FA’s

A

2 Extra Enzymes (Isomerase and Reductase) to modify double bonds

160
Q

Epinephrine

A

Stimulates Glycogenolysis in Skeletal Muscle/Liver; Stimulates Lipolysis

161
Q

Energy resevoir of Cardiac Muscle

A

Glycogen (few reserves)

162
Q

End Products of Lipolysis

A

Acetyl CoA, Glycerol

163
Q

Effect of Palmitoyl CoA on Acetyl CoA Carboxylase

A

Decreases rate of transcription -> Slows FA Synthesis

164
Q

Effect of Malonyl CoA on CPT1

A

Malonyl CoA inhibits CPTI, decreasing KB synthesis

165
Q

Effect of Low OAA levels of Ketogenesis

A

Diverts AcCoA into Ketogenesis from TCA; Rate of Citrate Synthase reaction reduced

166
Q

Effect of Low ATP/High AMP on Acetyl CoA Carboxylase

A

Activates PK that phosphorylates (deactivates) -> Inhibit FA Synthesis

167
Q

Effect of Insulin on Beta-Oxidation

A

Increase Malonyl CoA, Decrease Beta-Oxidation

168
Q

Effect of Insulin on Acetyl CoA Carboxylase

A

Stimulates dephosphorylation (activation) -> Promotes FA Synthesis

169
Q

Effect of High NADH/FADH2 on Beta-Oxidation

A

Inhibits

170
Q

Effect of High NADH on Ketogenesis

A

High NADH depletes OAA to help shunt AcCoA to make KB’s b/c less OAA is available for Citrate

171
Q

Effect of High NADH levels on Ketogensis

A

Converts OAA into Malate, which causes shunting of AcCoA into Ketogenesis instead of TCA Cycle

172
Q

Effect of High ATP on Ketogenesis

A

(1) High ATP = Less NADH Oxidized; (2) NADH/NAD+ ratio increases; (3) OAA converted to Malate; (4) AcCoA diverted from TCA to Ketogenesis, b/c of low OAA levels

173
Q

Effect of Glucagon on F-2,6-BisP

A

Decreases, Slows Glycolysis

174
Q

Effect of Citrate on Acetyl CoA Carboxylase

A

Increases rate of transcription -> Promotes FA Synthesis

175
Q

Effect of AMP-PK (muscle,liver) on Beta-Oxidation

A

Decrease Malonyl CoA, Increase conversion of Fatty Acyl CoA to Fatty Acyl Carnitine

176
Q

During what state is Urea production highest

A

Fasting, then protein breakdown slows

177
Q

Difference b/t Bile Salts and Cholesterol precursor

A

Rings in Bile Salts contain more Hydroxyl Groups, a polar side chain, Lack a 5-6 double bond

178
Q

Diff b/t FA elongation vs synthesis?

A

Elongation occurs while FA is bound to CoA, rather than to ACP

179
Q

Cortisol

A

Gluconeogenesis, AA Mobilization, Lipolysis

180
Q

Components of MTP

A

PDI, a chaperone; and TG Transfer portion

181
Q

Citrate Synthase

A

OAA to Citrate, Using Acetyl CoA

182
Q

Citrate Shuttle

A

Citrate out of Mito, Pyruvate in (Shuttling Acetyl CoA out for FA Synthesis)

183
Q

Citrate Lyase

A

Citrate to OAA using ATP, Producing Acetyl CoA for FA Synthesis

184
Q

Cholesterol Esters in Lipoproteins

A

OH group esterfied to a FA; Found in interior of Lipoprotein

185
Q

Carrier of FA Synthesis vs Beta-Oxidation

A

Protein (ACP) vs Coenzyme A

186
Q

Carnitine Deficiency

A

Inability to transport LONGCHAIN FA’s into mitochondria

187
Q

Carnitine Cycle

A

Exchange of Carnitine and Acyl Carnitine; Long Chain FA’s into mitochondria

188
Q

Cardiac Fuels

A

Primarily FA’s; Will use KB’s over Glucose

189
Q

cAMP and Lipolysis

A

Increased cAMP activates Lipase, increasing Lipolysis in Adipose tissue

190
Q

Apo B in Liver vs Intestine

A

Same gene; RNA Editing; Instestinal version (B-48) is half the size

191
Q

Antilipolytic Hormones

A

Insulin

192
Q

Acyl CoA “Desaturases”

A

ER; Contain FAD, Cytochrome B5, and an Iron-Sulfure Center; Various specificities, <10

193
Q

Activities affected by MTP loss

A

Chylomicron and VLDL assembly, both need an apoB protein to assemble

194
Q

Actions of MTP

A

Required to transfer lipid to apoB-48, and to transfer lipid from cytoplasm to ER lumen; Helps recruit TG lipid droplets as particle grows

195
Q

Actions of Lipolytic Hormones

A

Increase adipose cAMP and activate Lipase

196
Q

Action of Pancreatic Lipase

A

Cleaves FA’s from positions 1 and 3 of TG, producing 2 FA’s and a 2-MG

197
Q

Action of LPL

A

Breaks down TG’s to FA’s; FA’s taken into Adipose Cells

198
Q

Action of Gastric and Linguinal Lipases

A

Hydrolyze short/medium chain FA’s from TG’s

199
Q

Action of Carnitine in Mitochondrial Long-Chain FA Metabolism

A

Transports activated Fatty Acyl CoA into mitochondria

200
Q

Action of Beta-Hydroxybutyrate

A

Interconverts Acetoacetate and Beta-hydroxybutyrate

201
Q

Action of ApoE

A

Binds to receptors (in liver) that uptake chylomicron remnants

202
Q

Abetalipoproteinemia

A

Loss of TG Transfer Activity (MTP); Inability to take in and distribute dietary fats

203
Q

5 Steps of FA Synthesis

A

(1) Transfer of Malonyl; (2) Condensation of malonyl; (3) Reduction of beta-ketoacyl group; (4) Dehydration forms double bond; (5) Reduction of double bond w/ NADHP

204
Q

2-Carbon Donor of Elongation and Reducing Agent

A

Malonyl CoA, NADPH

205
Q

2 Steps of FA Activation

A

(1) ATP added to form high-energy Fatty Acyl AMP; (2) AMP is exchanged for CoA (product is Fatty Acyl CoA

206
Q

2 Sources of NADPH for FA Synthesis

A

Pentose Phosphate Pathway, Malic Enzyme (Malate to Pyruvate)

207
Q

2 Components needed for TG Synthesis in Adipose

A

Glycerol-3-Phosphate from Glucose and FA’s from VLDL’s

208
Q

1 Main difference b/t Ether Lipid and other Glycerolipids

A

Ether instead of Ester bond at C1

209
Q

2 Mechanisms to Add Head Group to Phosphatidic Acid

A

(1) Activate Head group with CTP; (2) Activate DG w/ CTP

210
Q

2 Starting components of Ceramide Synthesis

A

Palmitoyl CoA and Serine

211
Q

2 Types of Ether Glycerolipids

A

Plasmologens and PAF

212
Q

3 Components to make Phosphatidic Acid

A

Glycerol-3-P, 2 FA-CoA

213
Q

3 Steps of TG Synthesis

A

(1) Glycerol-3-P from Glycerol or Glucose; (2) Glyc-3-P -> Phosphatidic Acid; (3) PT Acid -> DG -> TG

214
Q

4 Types of Glycolipids

A

Cerebrosides, Sulfatides, Globosides, Gangliosides

215
Q

ABO blood groups are determined by what type of lipids

A

Sphingolipids

216
Q

Action of Pancreatic Lipase and Colipase

A

Hydrolyzes TG and DG, forming 2-MG and 2 FA’s

217
Q

Alpha-Galactosidase deficiency

A

Fabry Disease

218
Q

Backbone of Sphingolipids and Glycolipids

A

Ceramide, not Glycerol

219
Q

Beta-glucocerebrosidase deficiency

A

Gaucher Disease

220
Q

Ceramide

A

Sphingosine linked to FA at 2 w/ amide

221
Q

Ceramide backbone with carbohydrate group attached

A

Glycolipids

222
Q

Common Intermediate of Membrame Phospholipid Synthesis

A

Phosphatidic Acid

223
Q

Components of Cardiolipin

A

Phosphotidylglycerol and CDP-DAG

224
Q

Components of Glycerophospholipids

A

Glyercol, 2 FA, “Head Group”

225
Q

Degradation of Sphingolipids

A

Occurs in Lysosomes

226
Q

Difference b/t Plasmalogen and PAF

A

At C1: Unsaturated vs Saturated; At C2: Acyl vs Acetyl; At C3: Head group Ethanolamine vs Choline

227
Q

Diglyceride Acyltransferase is part of what complex?

A

TG Synthetase

228
Q

Ether Glycerolipid vs Glycerophospholipid

A

Ether bond at C1 instead of ester bond to FA

229
Q

Fabry Disease

A

Alpha-Galactosidase Deficiency; Accumulation of Globosides

230
Q

From what is Arachidonic Acid derived?

A

Phospholipids

231
Q

From what other phospholipid can you make phosphotidylserine

A

phosphotidylethanolamine (reversive exchange)

232
Q

Functions of Glycolipids

A

Cell recognition, Protective effects, Binding site for some toxins

233
Q

Ganglioside

A

Ceramide - Sugars - NANA

234
Q

Gaucher Disease

A

Beta-glucocerebrosidase deficiency; Ceramide-glucose not broken down; Accumulate Glucocerebroside

235
Q

General purpose of Sphingolipids

A

Help cell-cell, cell-matrix interactions

236
Q

Globosides

A

Ceramides attached to 2 or more sugars

237
Q

Glycerolneogenesis during Fasting

A

Adipose tissue can use Lactate, Pyruvate, & AA to regulate FA release; Gluc-3-P -> DHAP -> Glyercol-3-P

238
Q

Glycolipid Structure

A

Ceramide backbone with Carbohydrate group attached

239
Q

Head group of Phosphatidic Acid

A

H

240
Q

Head group of Phosphatidylcholine

A

Choline

241
Q

How is Glycerol-3-P produced in Adipose tissue normally?

A

Glucose -> DHAP -> Glycerol-3-P (using NADH)

242
Q

How is Glycerol-3-P produced in Liver?

A

Glycerol Kinase phosphorylates; Glucose to DHAP to Glycerol-3-P (Using NADH)

243
Q

How many high energy Phosphates are necessary to activate a FA?

A

2, ATP -> AMP

244
Q

How many hydrocarbon tails does PC have?

A

2

245
Q

Inability to degrade Glycolipids and Sphingomyelin in membranes

A

Mucolipidosis

246
Q

Neutral Glycolipids

A

Contain one or more sugars

247
Q

Phenotype w/ Glycerolneogenesis Pathway KO

A

Release abnormally high FA in blood in fasting and have low fat stores

248
Q

Phosphotidylethanolamine to Phosphotidylcholine

A

Add three Methyl Groups (3 SAM’s)

249
Q

Plasmologen locations

A

Mitochondria, Myelin, Muscle

250
Q

Polar head group of Ceramides

A

Don’t have one

251
Q

Polar head group of Glycolipids

A

Carboydrate

252
Q

Product when Dephosphorylate Phosphatidic Acid

A

DAG

253
Q

Requirements for Ceramide synthesis

A

Serine, PalmitoylCoA, FACoA, NADHP, FAD

254
Q

Structure of Ether Lipid (Plasmolgen)

A

Ether bond at 1 to Long Chain Alcohol (Double bond b/t carbons 1 and 2); FA at 2; Polar Head Group at 3

255
Q

Subcellular Location of TG Synthetase Complex

A

ER

256
Q

Sulfatide

A

Ceramide attached to sulfated galactose

257
Q

Synthesis of Sphingomyelin from Ceramide requires what?

A

Addition of Choline from Phosphatidylcholine

258
Q

T/F: Distribution of complex lipids is PM is symmetric

A

FALSE

259
Q

T/F: Glycolipids contain a phosphate

A

FALSE

260
Q

Tay-Sachs Disease

A

Hexosaminidase A Deficiency; GM2 Ganglioside Accumulates

261
Q

Tissue with Glycerol Kinase

A

Liver

262
Q

Type of Complex Lipid with Carbohydrate

A

Glycolipid

263
Q

Type of Plasmalogen in Heart Muscle

A

Choline Plasmologen

264
Q

Type of Plasmalogen in Myelin

A

Ethanolamine

265
Q

What 2 components make Sphingosine

A

Palmitoyl CoA and Serine

266
Q

What activates sugars in Glycolipid Synthesis

A

UDP or CMP

267
Q

What causes Mucolipidosis

A

Inability to degrade Glycolipids and Sphingomyelin in membranes

268
Q

What cells secrete LPL and in response to what?

A

Adipose, Insulin

269
Q

What determines type of Glycolipid

A

Nature of carbohydrate

270
Q

What do Sphingophospholipids and Glycolipids share?

A

Sphingosine backbone the 2-FA links by an Amide

271
Q

What does Inisitol react with to form PI?

A

CDP-DG

272
Q

What does synthesis of Glycerolipids require

A

NADPH, AcylCoA, DHAP, and activated Ethanolamine

273
Q

What drives the reaction of Phosphatidic Acid to Glycerophospholipids

A

CTP

274
Q

What helps sulfate Glycolipids

A

PAPS

275
Q

What is the 2-fatty acid replaced by in PAF

A

Acetyl Group

276
Q

What links FA’s in Sphingolipids/Glycolipids

A

Amide, not ester or ether

277
Q

What membrane is enriched with Cardiolipin?

A

Inner Mito Membrane

278
Q

Where are Glycolipids predominate

A

Neural Cells

279
Q

Where does synthesis of Glycolipids occur?

A

ER and Golgi (sugars sequentially added as activated glycosyl residues)

280
Q

Where is PAF made?

A

Peroxisomes

281
Q

Where is sphingomyelin enriched?

A

CNS along w/ Glycolipids

282
Q

Which Complex Lipids do not have Polar Head Groups

A

Glycolipids and TAG’s

Molecular Block 4 (2 decks)

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