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lipids Flashcards

1
Q

what are lipids?

A

heterogeneous group of biological compounds, including fats, oils, steroids, waxes, that are relatively insoluble in water

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2
Q

what are common properties of lipids?

A
  • relatively insoluble in water
  • soluble in nonpolar solvents
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3
Q

what are the functions of lipids?

A
  • energy storage
  • important dietary components because of their high energy
  • structural components of biomembranes
  • serve as thermal insulators in subcutaneous tissues and around certain organs
  • signaling molecules
  • hormone precursors
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4
Q

what are some clinical consequences of dyslipidemias?

A
  • tend to accumulate in joints
  • atherosclerosis, which can lead to stroke and heart attack
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5
Q

what are the different types of dietary lipids?

A
  • purifies lipids: triacylglycerols – neutral lipids (completely hydrophobic)
  • cellular lipids: lipid droplets (triacylglycerols, cholesterol esters), and membrane lipids (phospholipids, cholesterol, glycolipids)
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5
Q

how are dietary lipids absorbed (path from liver to small intestine)?

A
  • liver generates bile salts, which generate micelles
    -when in small intestines, pancreatic lipase hydrolyzes the triacylglycerols into free fatty acids and monoglycerides
  • i-FABP carries fatty acids inside the enterocytes, where they are converted back into triacylglycerols
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6
Q

how are dietary lipids transported from the enterocyte into the circulation?

A

the fatty acids and MAG are converted into triacylglycerols then packaged into chylomicrons, where they can be secreted into the circulation

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7
Q

where are free fatty acids located?

A

mitochondrion and cytosol

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8
Q

what is the structure of a fatty acid?

A
  • carboxylic acid with a long hydrocarbon chain
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9
Q

what is the difference between saturated and unsaturated fatty acids?

A
  • saturated: all carbon bonds are single bonds
  • unsaturated: has at least 1 double bond
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10
Q

which has a higher melting point, cis-unsaturated or trans-unsaturated?

A

cis

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11
Q

how is melting point affected by saturated and unsaturated FAs?

A
  • satur: longer has higher melting point
  • unsat: more unsaturation lowers melting point
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12
Q

how are branched FAs different from other types?

A
  • undergoes alpha-oxidation (peroxisome) instead of beta-oxidation (mitochondria)
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13
Q

what is the structure of triacylglycerols? how are they stored?

A
  • 3 acyl chains with 1 glycerol (100% hydrophobic)
  • in vesicles
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14
Q

what is the structure of phospholipids? how are they stored?

A
  • glycerol/sphingosine with 3 acyl chains
  • part of the membrane
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15
Q

how are endogenous TGs transported into the blood?

A

by VLDL

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16
Q

where are TGs located?

A

lipid storage droplets

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17
Q

what are the steps of TGs to energy (exogenous and endogenous)?

A

exo:
1. synthesized
endo:
1. ingested
2. transported
3. stored
4. mobilized to generate energy

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18
Q

Explain lipolysis in the GI-tract. (Enzyme used, when it occurs, regulation)

A
  • occurs in fed state
  • pancreatic lipase breaks down TGs
  • regulated by substrate availability
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19
Q

How can a charged FA traverse the non-polar membrane bilayer?

A
  1. Diffusion
  2. Transport
  3. Acidification of Pinochet of vesicle (extra cellular fluid has pH~7 so FA in charged state, internalized Pinochet if vesicle has pH~5 so FA neutral, FA can now diffuse across membrane, and cytoplasm has pH~7 so FA back to charged state)
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20
Q

Explain lipolysis in blood vessels (when it occurs, enzyme, regulation).

A
  • occurs in fed state
  • lipoprotein lipase breaks down TGs into FAs
  • LPL coats endothelial cells
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21
Q

What are the differences between the lipid droplets in the adipocyte and the liver?

A
  • adipocyte function is to store large amounts of TGs as fat droplets, so almost fills cell
  • liver has much smaller lipid droplets and serve as transient buffer reservoir of esterified FAs and esterified cholesterol
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22
Q

Explain lipolysis in lipid droplets (when it occurs, enzyme, regulation).

A
  • occurs when fasting or during exercise
  • 3 enzymes: TAG to DAG by ATGL, DAG to MAG by HSL, MAG to glycerol by MGL
  • the FAs released either go to blood (bounded by albumin), go to target or used immediately
  • regulation: hormonal regulation - PKA (activated by adrenaline) phosphorylates perilipin (coats droplets) and HSL which activates the pathway
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23
Q

Where does lipogenesis occur?

A

In enterocyte (liver)

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24
Q

Explain lipogenesis in enterocyte.

A
  • a fatty acid is activated by CoA via Acyl-CoA synthase, which makes a high energy intermediate Acyl-CoA
  • in process there is inorganic pyrophosphatase activity, which drives the reaction
  • we then take 2-monoacylglycerol (from diet) and we can then add the Acyl-CoA to make DAG
  • can then add another Acyl-CoA to make TAG
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25
Q

How is lipogenesis in enterocyte regulated?

A

Substrate availability

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26
Q

Where does TAG de novo synthesis occur?

A

In lipid droplets in liver and adipose

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27
Q

Explain TAG de novo synthesis.

A
  • glycerol-3-phosphate generated by PPP pathway ( so either DHAP to glycerol-3-P or glycerol to glycerol-3-P — 2nd can only occur in liver)
  • addition of 2 acyl-CoAs to make phosphatidic acid
  • dephosphorylation by lipin makes DAG
  • addition of 1 acyl-CoA makes TAG
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28
Q

How is lipogenesis regulated?

A

By insulin via transcriptional control

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29
Q

What happens in fed state?

A
  1. Lipolysis (pancreatic lipase)
  2. Re-assembly
  3. Transport (via chylomicrons)
  4. Lipolysis (LPL)
  5. Lipogenesis (in lipid droplets)
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30
Q

What happens in fasting or excessive state?

A
  1. Lipolysis (in lipid droplets)
  2. Transport (via albumin binding)
  3. Uptake in tissue
  4. Beta-oxidation (makes ATP)
31
Q

what are the different membrane lipids?

A
  • glycerolphospholipids
  • sphingolipid
  • glycolipids
  • sterols
32
Q

what are the differences between glycerophospholipids and sphingolipids?

A
  • glyc: FAs bound to phosphate group by glycerol, type of FAs may change
  • sphi: FA bound to phosphate by amide, FA always the same
33
Q

what are the role of membrane lipids?

A
  • in/out symmetry
  • microdomains (RAFTs are thick and stiff and non-rafts are thin and fluid)
  • signaling (e.g. PI)
34
Q

where does phospholipid synthesis occur?

A

ER

35
Q

how are PI, PG, and cardiolipin synthesized?

A
  • activation of phosphatidic acid by CDP-diacylglycerol synthase to make CDP-diacylglycerol (pyrophosphatase activity drives reaction)
  • addition of inositol for PI, or glycerol 3-P for PG and cardiolipin
36
Q

how are PE and PC synthesized?

A
  • prime head group (either choline or ethanolamine) with ATP (addition of P)
  • activating the head group by CTP (pyrophosphatase activity drives reaction)
  • addition of DAG
37
Q

how is PE converted to PC and where does this occur?

A
  • occurs in liver
  • get methyl groups from “one-carbon pathway”
  • addition of 3 methyl groups to N of PE to make PC by PEMT
38
Q

what is the one carbon pathway?

A
  • ATP added to methionine (pyrophosphate released)
  • makes 5-adenosyl-methionine, which has a sulfonium that is unstable to likely to release methyl group
39
Q

which function is highly dependent on abundant PC production and what happens if there isn’t enough?

A
  • synthesis of bile
  • gallstones
40
Q

how is PS synthesized?

A
  • transferase removes ethylamine and adds serine to make PS
  • is reversible reaction, so decarboxylase can re-make PE
41
Q

how are sphingolipids synthesized?

A
  • addition of an activated acyl to the serine backbone (makes ceramide)
  • transferring a phosphocholine head group to make sphingomyelin
  • OR addition of glucose head group to make glycosphingolipid
42
Q

where are phospholipases located?

A

plasma membrane

43
Q

what are the roles of phospholipases?

A

cleave phospholipids to:
- generate signaling molecules
- convert phospholipids to another
- modulate the shape of the plasma membrane (production of monoacylchain phospholipids, which have a cone shape)

44
Q

where does beta-oxidation occur?

A

mitochondria

45
Q

where do FAs come from (for FA breakdown)?

A
  • uptake from circulation
  • lipolysis
  • phospholipases (PLA)
46
Q

how are FAs transported into the mitochondria?

A
  1. FAs are activated by CoA via Acyl-CoA synthase (pyrophosphate activity)
  2. coupling to Carnitine via Carnitine palmitoyl transferase I (CPT I)
  3. transit toward the mitochondrial matric via carnitine/acylcarnitine translocase (so carnitine regenerated)
  4. FA released into the matrix via carnitine palmitoyl transferase II (CPT II)
47
Q

what is the rate-limiting step/enzyme of FA breakdown? how is it regulated?

A
  • CPT I
  • inhibited by malonyl-CoA since high concentration means high-energy state and need to activate FA biosynthesis
48
Q

explain beta-oxidation of saturated FAs? what are the products?

A
  • dehydrogenation (makes double bond between two CHs after COOH)
  • hydration (addition of OH)
  • dehydrogenation (makes C=O)
  • thiolic cleavage (removes the end - makes acetyl-coA)
  • repeat
  • each cycle (removal of 2 carbons) makes: 1 FADH2, 1 NADH, 1 acetyl-coA
49
Q

explain beta-oxidation of unsaturated FAs. what are the products?

A
  • the saturated portion broken down like normal
    for the unsaturations:
  • isomerization (moves double bond to two CHs next to COOH)
  • hydration (addition of OH)
  • dehydrogenation (makes C=O)
  • thiolic cleavage (removes the end - makes acetyl-coA)
  • repeat
  • each cycle (removal of 2 Cs) makes: 1 NADH, 1 acetyl-coA (no FADH2 produced)
50
Q

explain beta-oxidation for polyunsaturated FAs (even and odd). What are the products?

A
  • odd unsaturation: same as mono-unsaturation (no FADH2 produced)
  • even unsaturation: FADH2 produced but costs 1 NADPH
  • both produce 1 NADH and 1 acetyl-coA
51
Q

explain beta-oxidation of odd-chain FAs.

A
  • normal until the last 3 carbons
  • last 3 released as propionyl-CoA
  • propionyl-CoA converted to succinyl-CoA
  • succinyl-CoA joins the CAC
52
Q

explain beta-oxidation of branched FAs.

A
  • normal for unbranched carbons
  • branched carbons released as propionyl-CoA (which is converted to succinyl-CoA)
53
Q

where does ketogenesis occur?

A

liver

54
Q

when and why does ketogenesis occur?

A

occurs when:
- during fasting or starvation
- oxaloacetate is depleted (CAC stops)

why:
- ketone bodies serve as a shuttle for acetyl-CoA, which can be used by other tissues (like brain and heart) to make acetyl-CoA for energy

55
Q

explain ketogenesis.

A
  • 2 acetyl-coAs releases 1 acetate
  • rest converted to 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) intermediate
  • then converted to acetoacetate, which can be converted to acetone or hydroxybutyrate
56
Q

where does FA synthesis occur?

A

cytosol

57
Q

how is acetyl-coA transported to the cytosol?

A

by citrate shuttle:
- acetyl-coA converted by citrate by citrate synthase (CAC)
- citrate can go to cytosol
- citrate lyase converts it back to acetyl-CoA (which also regenerates oxaloacetate)

58
Q

explain FA synthesis. what is the rate limiting step?

A
  1. Acetyl-CoA converted to malonyl-CoA by acetyl-CoA Carboxylase (ACC), which is a irreversible, rate-limiting step of the synthesis. (ATP breakdown provides energy)
  2. Malonyl/Acetyl-CoA Transacylase (MAT) couples acetyl-CoA and malonyl-CoA with ACP, which keeps them activated (and prevents leakage to other compartments) – “priming”
  3. Elongation: “primed” acetyl/malonyl-CoA bound together (requires 2 NADPH) by fatty acid synthase – addition of 2 carbons (malonyl-CoA keeps adding on) – cycles until it is long enough and ACP is released
59
Q

how much energy is needed to make FAs?

A

for addition of every 2 carbons need:
- 1 acetyl-CoA
- 2 NADPH
- 1 ATP

  • also there is an extra 1 acetyl-CoA that is needed to start the synthesis
60
Q

how is ACC (acetyl-CoA carboxylase) regulated?

A

allosteric:
- activated by citrate
- inhibited by FAs

Hormonal:
- insulin: stimulates glucose uptake and PDH (so more acetyl-CoAs produced)
- glucagon: inhibits (by PKA-mediated phosphorylation)

61
Q

how are desaturations made in FAs?

A

by desaturases (there are 4 different ones that exists in mammals)

62
Q

what is a lipoprotein?

A

a circulating lipid carrier composed of a neutral lipid core, a monolayer of polar surface proteins (phospholipids and cholesterol), and at least one apolipoprotein

63
Q

what are the different lipoproteins?

A
  • chylomicrons
  • VLDL
  • IDL
  • LDL
  • HDL
64
Q

what are apolipoproteins?

A

amphipathic proteins that insert in lipoproteins and serve as ligand for lipoproteins recognition and docking

65
Q

chylomicrons: when are they produced, what are the apo-proteins, how are they metabolized, and what are the target tissues?

A
  • produced from dietary lipids
  • ApoC, ApoE, ApoB-48
  • when go in bloodstream, ApoC bind LPL, which breakdown down TAGs into FAs, and the remnants make chylomicron remnant, which has no ApoC
  • FAs go to muscle and adispose
  • chylomicron remnant bind to liver through recognition of ApoE and Apob-48, where it is internalized and broken down (liver can then make bile acids and use cholesterol for other things)
66
Q

VLDL: where and why are they produced, what are the apo-proteins, how are they metabolized, and what are the target tissues?

A
  • produced by liver with the excess lipids that it receives from chylomicrons, acts as a vehicle to deliver lipids to adipose
  • have ApoC and ApoB100
  • when go in bloodstream, ApoC bind LPL, which breakdown down TAGs into FAs, and the remnants make IDL (FAs go to muscle and adipose)
  • IDL can either bind to liver or gets broken down into LDL by hepatic lipase
67
Q

LDL: how is it made, what is its role, what is its target tissue.

A
  • made by hepatic lipase acting on IDL
  • role is to carry cholesterol esters to target tissue
  • can go to liver but mostly peripheral tissue by ApoB100 receptor, which uptakes it via clathrin-coated vesicles
68
Q

what is the role of HDL?

A

to recycle the lipids (cholesterol) back to the liver, where it can be used to make bile salts

69
Q

how are HDL particles made?

A
  • excess cholesterol is engulfed by macrophages
  • ABCA1 forms pre-HDL, which is wrapped by ApoA-1, by flipping the cholesterol that is in inner layer of membrane to the outer (so acts as a transporter)
  • LCAT esterifies cholesterol (makes cholesterol esters), which creates a spherical HDL due to change in hydrophobicity (went from amphiphilic to hydrophobic)
  • maturation: CETP allows for the exchange of TGs and CEs between HDL and VLDL. they go with their concentration gradients, so TGs go inside HDL and CEs go inside VLDL
  • mature HDL can now bind ApoA-1 receptor on liver, where it unloads the TGs and CEs
70
Q

How is cholesterol synthesized? How much energy is required?

A

synthesized by mevalonate pathway:
- acetyl-CoA converted to 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) by ketogenesis
- HMG-CoA reductase converts HMG-CoA to mevalonate (requires NADPH)
- mevalonate eventually converted to a lipid anchor intermediate (Farnesyl pyrophosphate) – requires a lot of energy (ATP)
- converted to squalene
- squalene converted to cholesterol

36 ATP and 16 NADPH/cholesterol

71
Q

how is cholesterol synthesis regulated?

A
  1. energy state:
    - when in low energy state (high AMP/ATP), HMG-CoA reductase is shut of by phosphorylation – when low energy, not enough energy to spare to make cholesterol
  2. through gene regulation:
    - SREBP is transcription factor for HMG-CoA reductase and LDL-R
    - when low cholesterol: SREBP transported to Golgi, where can cleave transcription factors, which causes the induction of transcription
    - when high cholesterol: SREBP associated with cholesterol, so doesn’t go in Golgi
72
Q

what do statins do?

A

they are HMG-CoA reductase inhibitors so decrease cholesterol synthesis

73
Q

what are uses of cholesterol in the body?

A
  1. storage as cholesterol esters
  2. bile salts
  3. hormones
  4. vitamin D
74
Q

What happens after a meal (intake of glucose and TGs) at rest in the following: pancreas, liver, muscle, brain, heart, adipose tissue.

A

pancreas: glucose taken up, causes release of insulin

liver: glucose
1. glycogen synthesis
2. FA synthesis
3. TG synthesis
4. storage in lipid droplets and/or VLDL secretion
liver: lipids
1. TG synthesis
2. storage in lipid droplets and/or VLDL secretion

muscle: glucose
1. glycogen synthesis
2. FA synthesis
3. TG synthesis
4. storage in lipid droplets and/or VLDL secretion
muscle: lipids
1. TG synthesis
2. storage in lipid droplets and/or VLDL secretion

brain: glucose intake and CAC cycle + OxPhos
Heart: glucose intake and CAC cycle + OxPhos

adipose tissue: glucose
1. FA synthesis
2. TG synthesis
3. storage in lipid droplets
adipose tissue: lipids
1. TG synthesis
2. storage in lipid droplets

75
Q

What happens during exercise (glucose and lipid metabolism) in the following: liver, muscle, brain, heart, adipose tissue.

A

liver: glucose
1. glycogen breakdown (glucose released in circulation)
2. lactate intake (gluconeogenesis)
liver: lipids
1. lipolysis of TG in lipid droplets
2. FA export to blood

muscle: glucose taken in
1. CAC + OxPhos
2. glycogen breakdown
3. lactate formation, released in blood
muscle: lipids taken in
1. lipolysis of TG in lipid droplets
2. beta-oxidation of FA: used in CAC + OxPhos

brain: glucose intake and used for CAC + OxPhos
heart: glucose intake and used for CAC + OxPhos

Adipose: glucose: nothing
Adipose: lipids
1. lipolysis of TG in lipid droplets
2. FA export to blood

76
Q

What happens during prolonged exercise or starvation (glucose and lipid metabolism) in the following: pancreas, liver, muscle, brain, heart, adipose tissue.

A

pancreas: glucagon produced

liver: glucose (exported to blood)
1. gluconeogenesis
liver: lipid
1. lipolysis of TG in lipid droplets
2. FA export to blood
3. ketogenesis (ketone bodies exported to blood)

muscle: glucose – nothing
muscle: lipid (intake)
1. lipolysis of TG in lipid droplets
2. beta-oxidation of FA: used in CAC + OxPhos

brain: glucose and ketone bodies intake used for CAC + OxPhos
heart: glucose and ketone bodies intake used for CAC + OxPhos

adipose tissue: lipids
1. lipolysis of TG in lipid droplets
2. FA export to blood

BIOC 311 (7 decks)

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