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BIOL 302 Part 1 > Lipid Metabolism > Flashcards

Lipid Metabolism Flashcards

1
Q

lipids (3)

A
  • small, water insoluble containing fatty acyl groups, isoprenoid/sterol groups
  • usually soluble in organic solvents
  • amphipathic: often predominantly hydrophobic, but have polar hydrophilic regions
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2
Q

functions of lipids (4)

A
  • energy storage
  • cell membrane
  • signalling molecules
  • insulation
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3
Q

fatty acids (3)

A
  • carboxylic acids containing long hydrocarbon chain
  • can be saturated or unsaturated
  • vary in # of carbons, # of double bonds, configuration of double bonds (cis/trans) an position of double bon
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4
Q

saturated FA

A
  • FA with no double bonds
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5
Q

unsaturated FA

A
  • FA contains double bonds
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6
Q

nomenclature of FAs (4)

A
  1. total # of carbons
  2. total # of double bonds
  3. cis or trans double bonds
  4. position of double bonds in numerical order
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7
Q

what ending is used for protonated acids (not ionized)

A
  • “-ic acid”

- oleic acid

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8
Q

what ending is use for de-protonated (ionized) acids?

A
  • “-oate”

- oleate

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9
Q

what factors affect FA melting point? (3)

A
  • chain length
  • # of double bonds
  • trans fat or cis fat
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10
Q

how does chain length affect FA MP?

A
  • longer chain -> higher MP
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11
Q

how does the # of double bonds in FA affect MP? (2)

A
  • more double bonds -> lower MP

- double bonds introduce kinks in hydrophobic tails so the tails cannot pack as tightly

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12
Q

MP in trans FA vs cis FA

A
  • having cis double bonds -> lower melting temperature
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13
Q

what configuration are most double bonds in nature?

A
  • cis, trans that are products of incomplete hydrogenation cause cancer and heart disease
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14
Q

triacylglycerols (TAG or triglycerides) (2)

A
  • glycerol with all 3 -OH esterified with different or identical FAs
  • neutral fats
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15
Q

function of triacylglycerol (3)

A
  • main storage form of FA in animals:
  • FA are almost completely reduced (less oxygen) allowing harvest of more energy per gram than for carbohydrates
  • TAG is hydrophobic: can store more TAG in a given volume compare to glycogen
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16
Q

glycerophospholipids

A
  • composed of glycerol backbone linked to 2 FAs (C-1 and C-2) and a phosphoester linkage to phosphate and a polar alcohol group (C-3)
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17
Q

glycerophospholipid function

A
  • membrane lipid
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18
Q

sphingolipids

A
  • sphingosine as a base with head group attached by -OH and FA chain
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19
Q

sphingolipid function

A
  • membrane lipid
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20
Q

steroids (4)

A
  • molecule containing core of 4 fuses of rings (A-D)
  • A - C: 6 carbons
  • D: 5 carbons
  • planar geometry, rigid, and amphipathic
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21
Q

sterol

A
  • a steroid with a OH group on the C-3
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22
Q

waxes (2)

A
  • chemical esters of FA linked to long-chain alcohol

- highly hydrophobic

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23
Q

eicosanoids (2)

A
  • derived from arachidonic acid

- signalling molecule involved in inflammation

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24
Q

membranes

A

lipid bilayers

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25
Q

3 major types of lipids in membranes (3) and common characteristic

A
  • glycerophophoslipids
  • sphingolipids
  • sterols
  • all are amphipathic
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26
Q

permeability of membranes (2)

A
  • impermeable to big molecules and small, but polar molecules
  • permeable to gases and small hydrophobic molecules
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27
Q

fluid-mosaic model of membrane (3)

A
  • membrane is fluid lipid bilayer with proteins floating in it
  • proteins and lipids can diffuse freely, but rarely flip-flop from layer to layer
  • membrane has proper fluidity that needs to be maintained to ensure proper function
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28
Q

Tm

A

temperature at which phase transition occurs

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29
Q

T &laquo_space;Tm (2)

A
  • liquid ordered state (crystalline)

- membrane is too rigid

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30
Q

T&raquo_space; Tm (2)

A
  • liquid disordered state (liquid solid)

- membrane is too fluid

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31
Q

how do organisms adjust membrane fluidity (2)

A
  • bacteria can change FA composition of membrane lipids

- eukaryotes have sterols in membrane (cholesterol in animals)

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32
Q

cholesterol when T < Tm

A
  • cholesterol prevents tight packing of FA tails and prevents transition to semi-solid state
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33
Q

cholesterol when T > Tm

A
  • cholesterol prevents free rotation of FA tails (enhances tighter packing), preventing transition to fluid-like state
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34
Q

when does FA synthesis occur (2)

A
  • when there are excessive nutrients (carbs, lipids, proteins)
  • convert excessive nutrients to FA and store as TAG in adipose tissue
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35
Q

generally, how does FA synthesis occur

A
  • carbs and amino acids can be oxidized and degraded to acetyl-CoA, which is directly use to build FAs
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36
Q

where does FA synthesis occur (2)

A
  • main sites: liver, adipose tissue and mammary glands during breast feeing
  • located in cytosol (don’t need organelles)
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37
Q

What is the general mechanism for FA synthesis (2)

A
  • FAs synthesize by adding 2 carbons at a time in each cycle

- only use acetyl-CoA for first 2 carbons, remaining use “activated form”: malonyl-CoA

38
Q

what are the 4 main steps in each cycle of FA synthesis (4)

A
  1. condensation
  2. reduction
  3. dehydration
  4. reduction
39
Q

preparatory step of FA synthesis (3)

A
  • conversion of acetyl-CoA to malonyl-CoA using CO2 and ATP
  • enzyme: acetyl-CoA carboxylase (ACC)
  • irreversible second reaction step
40
Q

acetyl-CoA carboxylase (ACC)

A
  • initiates FA synthesis by converting acetyl-CoA to malonyl-CoA
41
Q

fatty acid synthase (FAS) in bacteria

A
  • each step is catalyzed by single enzyme
42
Q

fatty acid synthase (FAS) in vertebrates

A
  • consist of one polypeptide chain with 7 functional domains with different activities
43
Q

What are the 2 important reaction thiol groups of FAS

A
  • acyl carrier protein (ACP): long, flexible phosphopantetheine group (derived B5 vitamin) that contains reactive thiol group
  • cys residue side chain in beta-ketoacyl-ACP synthase (KS) domain that can bind acyl-groups
44
Q

what end does chain growth occur in FA synthesis?

A
  • carbonyl end; original acetyl group is at the end of the tail
45
Q

how many cycles of FA synthesis do mammals go through?

A
  • 7 cycles
46
Q

what happens after the 7 cycles of FA synthesis?

A
  • thioesterase (TE) hydrolyzes C16 (palmitate) from ACP
47
Q

how do you make an other even-chain FA after FA synthesis cycles?

A
  • it is done by a separate enzyme (sometimes called elongases) that extend a chain via the same mechanism
48
Q

how do you make a odd-chain FA after FA synthesis cycles?

A
  • synthesized by alpha-oxidation: removal of CO2 or by using propionic acid instead of acetate as a primer in FA synthesis
49
Q

in humans, where do most odd-chain fatty acids come from?

A
  • from dairy products that are produced by bacteria
50
Q

how do you make a branched chain FA after FA synthesis cycles?

A
  • mostly in bacteria, made by special branching enzymes
51
Q

how do you make unsaturated FAs after FA synthesis cycles? (2)

A
  • special enzymes called denaturases introduce double bonds

- humans lack enzymes to introduce double bonds beyond C-9

52
Q

which FAs are essential and why? (2)

A
  • linoleic and linolenic acids are essential

- they have double beyonds C-9, which is unable to be synthesized in humans

53
Q

what is the first step of lipid catabolism?

A
  • TAG in adipose tissue is broken down to glycerol and free fatty acids during starvation
54
Q

what is the second step of lipid catabolism? (2)

A
  • free FA are transported via bloodstream complexed with albumin
  • tissues pick up FA from bloodstream
55
Q

what is the third step of lipid catabolism? (2)

A
  • FA oxidation: FAs are broken down into acetyl-CoA
  • electrons from FA oxidation or from acetyl-CoA catabolism in Krebs cycle are “captured” in NADH/FADH2 form that go to ETC to produce ATP (oxidative phosphorylation)
56
Q

where does FA oxidation take place?

A
  • occurs in mitochondria of most tissues (except brain and RBCs)
57
Q

acetyl-CoA carboxylase (ACC) (2)

A
  • catalyzes committed step of FA synthesis

- regulated allosterically and hormonally

58
Q

how is ACC regulated allosterically? (2)

A
  • citrate activates ACC (more citrate = more acetyl-CoA for FA synthesis)
  • palmitoyl-CoA inhibits CoA (more palmitoyl-CoA = enough FA inside cell already, so less FA synthesis)
59
Q

how is ACC regulated hormonally?

A
  • hormones activate signalling cascades that lead to changes in phosphorylation status of ACC
  • regulated by glucagon, insulin, and ATP:AMP levels
60
Q

what is the activation of phosphorylated ACC?

A
  • inactive
61
Q

what is the activation of dephosphorylated ACC?

A
  • active
62
Q

when is glucagon released and how does it affect ACC regulation? (3)

A
  • glucagon is released when blood glucose is low (not enough energy)
  • glucagon binds receptor and activates signalling cascade that leads to activation of protein kinase A (PKA)
  • PKA phosphorylates ACC (inhibits)
63
Q

when is insulin released and how does it affect ACC regulation? (3)

A
  • released when blood glucose is high (lots of energy)
  • insulin binds to receptor and activates signalling cascade that leads to activation of phosphatase
  • phosphatase dephosphorylates ACC (activates it)
64
Q

how does ATP:AMP levels regulate ACC? (2)

A
  • low ATP: high AMP (low energy state) activates special enzyme, AMPK
  • AMPK phosphorylates ACC (inhibits FA synthesis)
65
Q

how is carnitine-acyl-transferase (CAT I) regulated?

A
  • malonyl-CoA allosterically inhibits CAT I, preventing beta-oxidation during FA synthesis
66
Q

how is beta-hydroxyacyl-CoA dehydrogenase regulated?

A
  • allosterically inhibited by NADH (product inhibition)
67
Q

how is thiolase regulated?

A
  • allosterically inhibited by acetyl-CoA (product inhibition)
68
Q

cholesterol

A
  • 27C molecule derive from acetyl-CoA
69
Q

functions of cholesterol (3)

A
  • maintaining proper membrane fluidity
  • precursor for steroid hormones
  • precursor for bile acids and salts
70
Q

what are cholesterol sources? (2)

A
  • exogenous: mainly animal, derived products

- endogenous: we can synthesize it de novo (from scratch)

71
Q

how do mammals break down cholesterol and consequences? (2)

A
  • mammals cannot break cholesterol all the way to acetyl-CoA (although some bacteria can use cholesterol catabolism for energy)
  • excessive amounts of cholesterol can be deposited on blood vessel walls and lead to atherosclerosis
72
Q

where does de novo synthesis of cholesterol occur? (2)

A
  • mainly in the liver

- some happens in the intestines

73
Q

HMG-CoA reductase? (2)

A
  • major point of regulation is HMG-CoA reductase

- regulated both locally and hormonally

74
Q

what are the 3 ways that HMG-CoA is regulated locally? (3)

A
  • transcription
  • translation
  • degradation
75
Q

sterol regulatory element (SRE) and SRE binding protein (SREBP) (3)

A
  • sequence of DNA before HMG-CoA reductase gene
  • binding of SREBP to SRE initiates transcription of HMG-CoA reductase
  • more SREBP enzyme = more cholesterol
77
Q

how is HMG-CoA regulated through transcription? (3)

A
  • SREBP is anchored in the membrane
  • when cholesterol levels are high, SREBP will stay anchored in membrane = no activation of transcription
  • when cholesterol levels drop, SREBP is released from the membrane and diffuses to membrane to start HMG-CoA transcription
78
Q

how is SREBP released from the membrane? (3)

A
  • ER membrane translocates to golgi
  • golgi action of two proteases release SREBP from membrane
  • free SREBP diffuses to nucleus
79
Q

how is HMG-CoA regulated through translation?

A
  • translation of HMG-CoA is inhibited by derivatives of mevalonate
80
Q

how is HMG-CoA regulated through degradation?

A
  • degradation of HMG-CoA reductase is stimulated by lanosterol (and 25-hydroxy-cholesterol)
81
Q

how is HMG-CoA regulated hormonally? (3)

A
  • HMG-reductase is activated by insulin induced dephosphorylation
  • HMG-redustase is inactivated by glucagon induced phosphorylation
82
Q

what are the cholesterol derivatives? (3)

A
  • cholesterol esters
  • bile salts and acids
  • steroid hormones
83
Q

cholesterol ethers: how is it related to cholesterol and function (2)

A
  • FAs can form esters with -OH of cholesterol making it more hydrophobic
  • allows storage and transports of cholesterol due to tighter packing
84
Q

how and where is cholesterol ester synthesized? (2)

A
  • synthesized in liver: by ACAT using FA-CoA

- in HDL particles: by LCAT using phosphatidyl choline

85
Q

bile salts and acids: (2)

  • definiton
  • purpose
A
  • polar derivatives of cholesterol
  • synthesized in the liver to help emulsify lipids in intestines and a way to excrete excessive cholesterol (not efficient and accumulation occurs)
86
Q

steroid hormones (3)

  • common precursor and # of classes
  • what it is
  • purpose
A
  • 5 major classes with common precursor: pregnenolone
  • more oxidized and compact than cholesterol
  • helps cholesterol to cross cell membranes and bind DNA or intracellular receptors
87
Q

characteristics of ACC

A
  • ACC has biotin (vitamin B7) as a prosthetic group that is attached to Lys residue in active site of ACC
88
Q

What are the sources of NADPH for FA synthesis? (2)

A
  • conversion of malate to pyruvate

- pentose phosphate pathway

89
Q

What are the sources of acetyl-CoA for FA synthesis?

A
  • carbohydrate and amino acid catabolism in the mitochondrial matrix
90
Q

how are unsaturated FA oxidized? (3)

A
  • enzyme: delta^2,delta^3-enoyl-CoA-isomerase
  • monounsaturated FA require isomerase to reposition the double bond to allow hydration
  • FADH2 is NOT produced, so there will be 1.5 less ATP produced
91
Q

how are odd-chain FA oxidized? (3)

A
  • broken down by same mechanism until 5C-acyl-CoA
  • 5C-acyl-CoA is broken down to acetyl-CoA and propionyl-CoA
  • propionyl-CoA is converted to succinyl-CoA (Kreb cycle intermediate) or used in gluconeogenesis
92
Q

how are long-chain FA oxidized?

A
  • oxidized in peroxisome until they are short enough to be transferred into mitochondria via carnitine shuttle

BIOL 302 Part 1 (4 decks)

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