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Biochemistry 316 : Metabolism > Topic 2: Lipid transport, structure, and metabolism > Flashcards

Topic 2: Lipid transport, structure, and metabolism Flashcards

1
Q

Classifications of lipids (5)

A 
Fatty Acid
Glyceryl esters
Sphingolipids
Sterol derivitives
Terpenes
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2
Q

Triglycerol structure

A

glycerol backbone

3 fatty acids

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3
Q

Types of phospholipids

2

A

Glycerophospolipids

Sphingolipids

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4
Q

glycerophospholipid structure

A

glycerol backbone
2x fatty acid
PO4-alcohol

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5
Q 
Sphingolipid structure
(2 types)
A

sphingosine backbone
fatty acid

(phospholipid version)
PO4-Choline

(glycolipid version)
Mono or oligosaccharide

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6
Q

types of glycolipids (2)

A

sphingolipids

galactolipids (sulpholipids)

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7
Q

galactolipid (sulpholipid) structure

A

glycerol backbone
2x fatty acid
mono or disaccharide-SO4

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8
Q

X group of phosphaditic acid (PA)

A

-H

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9
Q

X group of phosphaditylethanolamine (PA)

A

ethanolamine

-CH2CH2NH3+

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10
Q

X group of phosphatidylcholine (PC)

A

Choline

-CH2CH2N+(CH3)3

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11
Q

X group of phosphaditylserine (PS)

A

serine

-CH2CH(COO-)NH3+

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12
Q

X group of phosphatidylglycerol (PG)

A

glycerol

-CH2CH(OH)CH2OH

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13
Q

X group of phosphatidylinositol (PI)

A

myo-inositol 4,5 biphosphate

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14
Q

how to make sphingosine

A

attach a ser backbone and fatty acid (palmatate) to glycerol

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15
Q

X group of sphingomylein

A

phosphocholine

PO3CH2CH2N(CH3)3

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16
Q

X group of glucosylcerebrocyde

a sphingolipid

A

glucose

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17
Q

X group of lactosylceramide

a sphingolipid, (globoside)

A

di or trisaccharide

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18
Q

X group of ganglioside GM2

a sphingolipid

A

complex oligosaccharide

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19
Q

Double bonds and carbon length of palmitate

A

C16, 0 double bonds

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20
Q

Double bonds and carbon length of stearate

A

C18

0 double bonds

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21
Q

Double bonds and carbon length of oleate

A

C18

1 double bond

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22
Q

Double bonds and carbon length of linolate

A

C18

2 double bond

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23
Q

Double bonds and carbon length of linolenate

A

C18

3 double bonds

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24
Q

Linolate vs linolnate

A

Linolate has 2 double bonds
Linolenate has 3 double bonds
Both are C18 fatty acids

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25
Q

Double bonds and carbon length of arachidonate

A

C20

4 double bonds

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26
Q

Why is olestra not accessible by gut enzymes ?

A

The glucose backbone is not accessible by the enzymes.

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27
Q

2 medical problems associated with olestra

A

1) loss of fat soluble vitamins (ADEK)

2) olestra is not absorbed and therefore egested, leading to anal leakage

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28
Q

WHAT DID THE DEVELOPMENT OF THE FAT SUBSTITUTE OLESTRA REINFORCE IN OUR KNOWLEDGE ABOUT THE
A) SPECIFICITY B) EFFICIENCY OF PANCREATIC LIPASE ENZYMES?

A

Enzymes are rather specific to which backbones are accessible to them
Lipids are typically fully absorbed

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29
Q

WHAT ARE THE IMPLICATIONS OF THIS KNOWLEDGE (re: olestra) FOR NORMAL DIETARY LIPID ABSORPTION & ENERGY UTILISATION?

A

Lipids are typically absorbed and fully digested.

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30
Q

2 important fatty acids for infant development

A

linolate and linolenate

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31
Q

Common type of double bond in lipids

A

cis bonds

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32
Q

Cis double bonds create a ___ degree kink in the fatty acidq

A

30 degree

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33
Q

How to make a helical fatty acid

A

add a double bond every 3 carbons

eg docosahexaenoic acid (DHA)

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34
Q

main component of retinal membrane phospholipids

A 
50% 
docosahexaenoic acid  (DHA)

Found mostly in the myelin sheath

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35
Q

preferred form of fatty acid to store energy

A

saturated

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36
Q

fatty acid form preferred for position 2 of phospholipids

A

unsaturated

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37
Q

IF I FED YOU A LABORATORY DIET
RICH IN EITHER SATURATED OR UNSATURATED FATTY ACIDS, WOULD YOUR BODY
COMPOSITION CHANGE AND IF SO, HOW?

A

Fat depots would reflect dietary intake, but membranes would not

Membranes are controlled for fluidity

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38
Q

What is the limit to adding double bonds to fatty acids?

A

cannot add past C9

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39
Q

oleic acid structure

A

ω9

18:1 Δ9

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40
Q

linoleic acid structure

A

ω6

18:2 Δ9,12

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41
Q

linolenic acid structure

A

ω3

18:3 Δ9,12,15

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42
Q

how to get eggs to have omega 3 fatty acids

A

feed them flax

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43
Q

Where can enzymes insert double bonds in fatty acids?

A

they use 6-desaturase and 5 desaturase to insert between C-4 and C-9

44
Q

HOW DO WE GET FROM 18:2 Δ9,12 TO 22:5 Δ4,7,10,13,16 ?

A

You can add a 4 double bond with 6 desaturase and then beta oxidise

45
Q

HOW DO WE GET FROM 18:3 Δ9,12,15 TO 22:6 Δ4,7,10,13,16,19 (DHA)?

A 
6 desaturase
extend (add 2C)
5 desaturase
extend
extend
6 desaturase
beta oxidationq
46
Q

Lipoprotein that transports dietary fatty acids

A

chylomicrons

47
Q

3 types of lipases

A

Pancreatic
for digestion of dietary fat

Bloodstream
eg lipoprotein lipases

Hormone sensitive
in adiocytes for mobilizing fat stores

48
Q

Emulsifying agent for dietary lipids

A

bile salts

amphoteric

49
Q

Role of colipase on lipase

A

Colipase binds to lipase and opens the ‘lid’ exposing the active site

50
Q

what is a micelle ?

A

A monolayer of bile salts filled with triglycerides

51
Q

4 types of lipoproteins

A

clylomicrons
VLDL
LDL
HDL

52
Q

Chylomicron density

A

<1.006 g/mL

53
Q

VLDL density

A

0.95-1.006 g/ml

54
Q

LDL density

A

1.006-1.063 g/ml

55
Q

HDL density

A

1.063 - 1.210 g/ml

56
Q

why is LDL associated with high cholesterol ?

A

Lots of cholesterol is used in the membrane of LDL

57
Q

key coenzyme in chylomicron for lipoprotein lipase regocnition

A

apo-CII

58
Q

where would you find a apo-CII ?

A

It is a coenzyme found on the surface of a chylomicron and VLDL

59
Q

Difference between cholesterol and cholesteryl ester

A

cholesterol is amphipathic and will stay in the membrane

cholesteryl esters are entirely hydrophobic and will enter the centre of a chylomicron

60
Q

Locations of liporotein lipase

A

Peripheral tissues, adipose, muscle

61
Q

3 types of hormone sensing lipases

A

Adipocyte triacylglycerol lipase (ATGL)
TG-> FA + DG

Hormone sensitive lipase (HSL)
DG -> FA + MG

Monoacyl glycerol lipase (MGL)
MG -> FA + Glycerol

62
Q

regulation of hormone sensitive lipases is controlled by

A

glucose

cAMP / protein Kinase A mediated events

63
Q

why lipid is slow energy release

A

hydrophobic environment

enzymes can only get at the fat from the outside of adipocyte

64
Q

Hormones that trigger triclycerol breakdown (2)

A

glucagon

epinepherine

65
Q

WHAT IS THE METABOLIC FATE OF A FATTY ACID TAKEN IN AS PART OF THE DIET?

A

It will be digested and stored in the adipose tissue.

It may be used for energy or building blocks

66
Q

WHAT WOULD HAPPEN IF YOU INGESTED A PANCREATIC LIPASE INHIBITOR WITH YOUR BIG MAC?

A

It would inhibit the breakdown of dietary fats in the small intestine, and therefore inhibit absorption.

67
Q

Why is there a low free fatty acid content in the blood ?

A

The carboxyl end is rather reactive

68
Q

Can a fatty acid leave the mitochondrion ?

A

No. Once it enters, it cannot be exported

69
Q

bond between coenzyme A and fatty acid

A

thioester

(-SH + HOOC-R

70
Q

This enzyme attaches fatty acids to coA

A

thiokinase

71
Q

2 procedures driven by pyrophosphate breakdown

A

Fatty acid -> fatty acyl CoA

UDP glucose production

72
Q

Non covalently bound forms of fatty acid (2)

A

Albumin (blood) - has 7FA max

Fatty acid binding protein - clamshell

73
Q

3 parts of carnitine transport system

A

Carnitine AcylTransferase-I
Carnitine Transporter
Carnitine AcylTransferase-II

74
Q

6 steps of carnitine transport system

A

Thiokinase generates fatty acyl CoA in cytosol

Carnitine AcylTransferase-I
Attaches fatty acid from Fatty acyl CoA to carnitine

Pores (create by porin) in outer mitochondrial matrix allows fattyl adducts to pass into intermitochondrial space

Carnitine Transporter
Transport fattyAcyl carnitine across inner mitochondrial membrane
Exchanges it with free carnitine (antiport)

Carnitine AcylTransferase-II
Reattaches fatty acid to CoA-SH

Beta oxidation

75
Q

Permeability of mitochondrial membranes

A

the inner mitochondrial membrane is basically impermeable, but the outer is quite leaky

76
Q

Fatty acids carried by carnitine

A

long chain (C16 - C22)

77
Q

Carnitine derived from these amino acids

A

Lysine and methionine

78
Q

WHICH OF THE VARIOUS FATTY ACID FORMS THAT YOU HAVE LEARNED ABOUT INVOLVE COVALENT LINKAGES: CARNITINE, FATTY ACYL CoA , FABP, CHOLESTERYL ESTER, TRIGLYCERIDE, ALBUMIN?

A

CARNITINE, FATTY ACYL CoA, CHOLESTERYL ESTER, TRIGLYCERIDE

FABP (fatty acid binding protein) and albumin are the only ones that do not

79
Q

WHY DOES THE CELL NEED A FATTY ACID TRANSPORTER IN THE PLASMA MEMBRANE?

A

To allow fast and specific transport

80
Q

WHY ARE CARNITINE-DEFICIENT PATIENTS TREATED WITH MEDIUM CHAIN FATTY ACIDS?

A

carnitine transports long chain fatty acids, which a carnitine patient wouldn’t be able to handle.
Medium chain FAs use a different pathway.

81
Q

4 steps to beta oxidation

A

oxidation
hydration
oxidation
clevage

82
Q

Where does the energy come from in beta oxidation ?

A

the 2 oxidation steps produce reducing agents
(FADH2 and then NADH)

Acetyl coA is a product, which is fed into the TCA cycle

83
Q

what is produced by beta oxidation ?

A

Acetyl co A (2 carbons) and a shorter fatty acid

84
Q

How many water molecules come from one palmatate molecule ?

A

It produces 23, but one is required to remove it from the glycerol backbone

85
Q

Where is usable water produced in beta oxidation ?

A

Electron transport chain

86
Q

Regulation of beta oxidation

A

1) Substrate supply (main mechanism)
2) NADH inhibits 3-OH-CoA dehydrogenase (3rd step)
3) Acetyl CoA inhibits thiolase (3rd step)

87
Q

main difference between mitochondrial and peroxisomal beta oxidation

A

Aside from location : mitochondria vs peroxisome (glyoxisome in plants) ,
the FADH2 and NADH in peroxisomal β oxidation is recycled without electron transport chain.

88
Q

What does ω-oxidation do?

A

Adds a carboxyl group on the omega end of a fatty acid so you can do beta oxidation from both sides
Makes adipate and/or succinate

89
Q

WHERE IS THE “USEABLE” WATER GENERATED IN THE β-OXIDATION OF FATTY ACIDS?

A

Electron transport chain

90
Q

COMPARE (2.5 MARKS) AND CONTRAST (2.5 MARKS) : FATTY ACID MITOCHONDRIAL β-OXIDATION, PEROXISOMAL β-OXIDATION & ω (OMEGA)-OXIDATION.

A

Aside from location : mitochondria vs peroxisome (glyoxisome in plants) ,
the FADH2 and NADH in peroxisomal β oxidation is recycled without electron transport chain.

omega oxidation takes place in the mitochondria, but adds a carboxyl group to the omega end without affecting the length

91
Q

WHAT IS SIGNIFICANT ABOUT THE ENTRY OF FATTY ACYL CoA INTO THE MITOCHONDRIAL MATRIX?

A

Once its in, its only fate is beta oxidation

If in the liver, it may undergo ketogenesis

92
Q

In well fed liver, what are the sources of acetyl coA and oxaloacetate ?

A

Acetyl CoA comes from fat, and the oxaloacetate is formed from pyruvaate

93
Q

In starving liver, where does oxaloacatate come from ?

A

Gluconeogenic precursors are mobilized to create pyruvate and oxaloacetate.
Adipose tissue is broken down to acetyl coA

Beta oxidation releases some energy, so TCA is not necessary.

94
Q

Where does the glucose come from during starvation ?

A

When glycogen stores are used up, anapleurotic steps are taken to produce oxaloacetate.
Oxaloacetate is then exported to make glucose

95
Q

Where to the ketone bodies come from during starvation ?

A

Fat deposits are broken down into Acetyl CoA

The Acetyl CoA is then used to make ketones

96
Q

How is the TCA cycle affected in the liver during starvation ?

A

It is shut down completely
All gluconeogenic precursors are used to make oxaloacetate, then glucose
Acetyl CoA from fat is used to make ketones
The liver gets all the energy it needs from beta oxidation

97
Q

Ketone bodies formed by the liver

A

Acetoacetate
D-β hydroxybutyrate
acetone*

*not used for energy (its a waste product)

98
Q

What tissues use ketones ?

A

In starvation, most tissues other than the liver (where it was made) will use ketones

99
Q

Where are ketones produced ?

A

The mitochondria of the liver

100
Q

When are ketones produced ?

A

Ketones are always being produced, but it happens especially during starvation

101
Q

Why can liver not use ketones ?

A

It does not have the 3-ketoacyl CoA transferase

102
Q

Why are ketones not prominent always ?

A

Ketones are acidic and will cause acidosis or death

103
Q

WHY DOES THE MYOPATHIC (MUSCLE-ONLY) TYPE HAVE NORMAL KETOGENESIS BUT FAT(TY ACID) ACCUMULATION IN MUSCLE?

A

Ketones are produced in the liver

Disabling fat transport in the muscle would not affect ketogenesis

104
Q

WHERE DOES THE STARVING LIVER GET ITS ENERGY?

A

The oxidizing steps of beta oxidation produce reducing agents for the electron transport chain

105
Q

WHY DOES THE BRAIN ADAPT TO USING KETONE BODIES DURING STARVATION NOT USE FATTY ACIDS?

A

ketones are smaller than fatty acids and polar

They can therefore cross the blood brain barrier

Biochemistry 316 : Metabolism (7 decks)

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