Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MTC Block 2: Post Quiz Material > 3- Fatty Acid Metabolism > Flashcards

3- Fatty Acid Metabolism Flashcards

1
Q

Classifications of lipids

A 
Storage lipids (neutral) 
1. Triacylglycerols

Membrane lipids (polar)

  1. Phospholipids
    - glycerophospholipid
    - sphingolipid
  2. glycolipids
    - sphingolipds
    - galactolipids (sulfolipids)
  3. archeabacterial ether lipids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

tricylglyerols

A

glycerol with 3 fatty acids attached

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

lipids that do not contain fatty acids

A

cholesterol

if they contain them then they are “complex lipids”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why are fatty acids physiologically important?

A
  1. building blocks of phospho and glycolipds
  2. important amphipathic part of biological membrane
  3. post-translational modification: covalent attachment to many proteins target these proteins to membrane locations
  4. important source of energy (triglycerides) stored in adipose tissue
  5. fatty acid derivatives are hormones and intracellular messengers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are fatty acids

A

hydrocarbon derivatives that consist of an alkyl chain (4-36 carbons long) with terminal carboxyl group

  • most common ones have EVEN number of carbons
  • common in humans: C16 (palmitate), C18 (sterate), C20 but longer ones are typically in nervous system (nervonic acid- sphingolipid) makes myelin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

saturated fatty acid

A

no double bonds

CH3 - (CH2)n - COOH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

unsaturated fatty acid

A
  • can have up to 6 double bonds per chain
  • they are almost always cis configuration which puts a kink into the alkyl chain
  • never directly next to each other but maybe one methylene b/w each double bond group
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

palmitate / palmitic acid

A

C16

16:0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

stearate / stearic acid

A

C18

18:0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

nomenclature of fatty acids

A

chain length: number of double bonds

  • start counting carbons at carboxyl then move down and the last carbon is called an omega carbon
  • if it says “omega” in the name then count from the other end (not carboxyl)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

palmitoleic acid

A

C16

16:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

oleic acid

A

C18

18:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

arachidonic acid

A

20: 4 fatty acid

- key omega 6 fatty acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Essential fatty acids

A

polyunsaturated fatty acids (PUFAs) cannot be synthesized in body and must be obtained by dietary sources –> humans lack desaturase enzymes required for their production

-endogenous synthesis may not attain same beneficial high levels as consumption in diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

name the two essential fatty acids

A
  1. Linoleic acid 18:2 (delta 9,12) –> omega-6 fatty acid
    - arachidonic acid
  2. a-linolenic acid 18:3 (delta9,12,15) –> omega-3 fatty acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

omega-3

A

a-linolenic acid 18:3

vegetable oils, nuts, seeds, shellfish, and fish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

omega-6

A

Linoleic acid 18:2

leafy vegetables, seeds, nuts, grains, vegetable oils, and meats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

name 2 key omega 3 and 1 key omega 6 fatty acids?

A

omega 3

  • eicosapentaenoic acid (EPA)
  • docosahexaenoic acid (DHA)
  • THESE 2 may be in baby formula cause they are important for NS development

omega 6
-arachidonic acid (important precursor for your prostaglandins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

biological functions of of omega 3 and 6 derivatives

A

eicosanoid synthesis- inflammation

endocannabinoids- mood, behavior, inflammation

imbalance b/w the two is associated with increased risk for CV disease (optimal is omega 6: omega 3 = 1:1 to 4:1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Non-essential fatty acids

A

no needed and dont need them from your diet

  • monounsaturated FA (lowers LDL)
  • saturated FA (raise cholesterol levels)
  • trans FA (raise LDL and lower HDL) —> trans is VERY bad for you
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why are trans fatty acids so bad?

A
  • form by partial dehydrogenation of unsaturated FA (done to increase shelf life or stability at high temperature of oils used in cooking- like deep frying)
  • trans double bond allows FA to adopt extended/straightened out conformation
  • trans can pack for tightly and have higher melting point than cis forms
  • consuming trans fats increases risk of CV disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what determines physical properties of fatty acids

A

length and degree of unsaturation of hydrocarbon chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

solubility of FA

A
  • poor solubility in water due to non-polar hydrocarbon chain
  • the longer the FA chain and the fewer the double bonds, the lower the solubility in water
  • more soluble = shorter with double bonds in chain
24
Q

melting points of FA

A
  • longer acids melt at higher temperatures
  • fully saturated FA have waxy consistency due to tighter packing in membrane
  • introduction of double bonds (desaturation) results in lower melting points, since kinks in chain dont allow for tight packing
  • these weaker interactions increase membrane fluidity (flexibility)- a good thing up to a point
25
Q

FA synthesis and palmitate

A
  • FA synthesis occurs in liver and cytosol of cells
  • process uses carbons from acetyl-CoA into growing FA chain using ATP and reduced NADPH
  • plamitic acid (16:0) is the first one to be synthesized then all others are made by its modification
26
Q

Step 1 of FA synthesis

A

Formation of malonyl-CoA

  • acetyl-CoA provides all carbons for FA and when palmitate is made then
  • BUT acetyl-CoA is in the mitochondrial matrix (working with pyruvate dyhydrogenase complex) and FA synthesis happens in the cytosol so you need a way to move acetyl Co-A to the cytosol.
27
Q

Step 2 of FA synthesis

-moving acetyl-CoA from the inner mitochondrial membrane to the cytosol so you can make malonyl-CoA with it

A
  • Citrate can be freely transported from mitochondrial matrix to cytosol by the TRICARBOXYLATE TRANSPORTER (Citrate transporter)
  • it is then converted back to oxaloacetate and acetyl-CoA by ATP-citrate lyase:

Citrate + ATP +CoASH —> oxaloacetate + Acetyl-CoA +ADP + Pi

28
Q

Step 3 of FA synthesis

A

Requirements: ATP, NADPH, CO2 (HCO3-)

COMMITTED STEP
-acetyl-CoA being caboxylated to malonyl-CoA by the enzyme acetyl-CoA carboxylase, which is also essential regulatory enzyme in this pathway

29
Q

Acetyl-CoA carboxylase

A
  • committed step of FA synthesis (carboxylates acetyl-CoA)
  • has 3 functional units, one that has a lysine residue which provides a “swinging arm effect”
  • this arm swings “activated CO2” to the acetyl-CoA to form malonyl-CoA
30
Q

what happens after step 3 of FA synthesis?

A
  • you end up with acetyl-CoA, malonyl-CoA, and NADPH in a repeating 4-step sequence
  • the fatty acyl chain is extended by 2C with each passage through the cycle
  • Fatty acid synthase complex catalyzes multiple cycles of condensation, reduction, dehydration, then another reduction for a fully saturated acyl group
31
Q

Fatty Acid Synthase Complex (FAS)

A

-used after first 3 steps in FA synthesis

  • single polypeptide chain with 7 active sites (function as distinct but linked enzymes)
  • direct transfer b/w sites
  • coordinate transcriptional regulation (1mRNA to make the whole complex)
  • when chain length reaches 16 carbons (palmitic acid) then it leaves the cycle…. needs 7 rounds in total to get to C16
  • thioesterase (TE) removes palmitate
32
Q

Acyl carrier protein (ACP) in FA synthesis

A

intermediates are linked to an ACP though a phosphopantetheine group/Pantothenic acid (very long flexible arm that carriers reaction intermediates from one enzyme active site to the next) attached to the ACP

-its the shuttle that holds everything together

33
Q

4 steps of FAS: STEP 1

A

-two thiol groups on FAS must first be charged with correct acyl group.

  1. Condensation
    - enzyme: ketoacyl-ACP synthase
    - malonyl-CoA to B-Ketobutyryl-ACP
  • malonyl-CoA is attached to ACP and acetyl Co-A is attached to a part of the FAS complex
    (product: ACP-Malonyl-acetyl)
34
Q

4 steps of FAS: STEP 2

A

malonyl-CoA to B-Ketobutyryl-ACP to B-hydroxygutyryl-ACP

  1. Condensation
    - enzyme: ketoacyl-ACP synthase
  2. Reduction of carbonyl group
    - enzyme: B-ketoacyl-ACP reductase (KR)
    - Ketobutyryl-ACP to B-hydroxygutyryl-ACP
    - uses NADPH has reducing agent (electron donor)
35
Q

4 steps of FAS: STEP 3

A

malonyl-CoA to B-Ketobutyryl-ACP to B-hydroxygutyryl-ACP to trans-delta2-butenoyl-ACP

  1. Condensation
    - enzyme: ketoacyl-ACP synthase
  2. Reduction of carbonyl group
    - enzyme: B-ketoacyl-ACP reductase (KR)
    - Ketobutyryl-ACP to B-hydroxygutyryl-ACP
    - uses NADPH has reducing agent (electron donor)
  3. Dehydration
    - enzyme: B-hydroxyhutyryl-ACP dehydratase (DH)
    - B-hydroxybutyryl-ACP to trans-delta2-butenoyl-ACP
36
Q

4 steps of FAS: STEP 4

A

malonyl-CoA to B-Ketobutyryl-ACP to B-hydroxygutyryl-ACP to trans-delta2-butenoyl-ACP to Butyryl-ACP

  1. Condensation
    - enzyme: ketoacyl-ACP synthase
  2. Reduction of carbonyl group
    - enzyme: B-ketoacyl-ACP reductase (KR)
    - Ketobutyryl-ACP to B-hydroxygutyryl-ACP
    - uses NADPH has reducing agent (electron donor)
  3. Dehydration
    - enzyme: B-hydroxyhutyryl-ACP dehydratase (DH)
    - B-hydroxybutyryl-ACP to trans-delta2-butenoyl-ACP
  4. Reduction of double bond
    - enzyme: enoyl-ACP reductase (ER)
    - reduces double bond of trans-delta2-butenoyl-ACP to form butyryl-ACP
    - uses NADPH as reducing agent (electron donor)
37
Q

Net reaction of FAS complex

A

8Acetyl-CoA + 7ATP + 14NADPH + 14H+ —> palmitate + 8CoA + 7ADP + 7Pi + 14NADP+ + 6H20

38
Q

Once you have made Palmitic acid through the first 3 steps then the repeated 4 step FAS, you may need to elongate some of the fatty acids

A
  • occurs inside mitochondria and on cytosolic face of smoothER membrane
  • these reactions add 2C at a time using fatty acyl-COA substrates
  • require malonyl-CoA (carbons) and NADPH (reducing power)
  • ER elongation prefers palmitoyl-CoA as substrate and produces stearate (18:0)
39
Q

How to desaturate fatty acids

A
  • synthesized in ER
  • palmitate and stearate serve as precursors of palmitoleic acid (16:1 deta9) and oleic acid (18:1 delta9)
  • committed step: stearoyl-CoA desaturase
40
Q

stearoyl-CoA desaturase

A

committed step which introduces a double cis double bond between C9 and C10

  • mammals lack desaturases to make linoleate and a-linolenate, so we need to eat these
  • once we eat these they can be converted to eicosanoids
  • play critical role in development of obesity and insulin resistance in Type 2 diabetes
41
Q

synthesis of eicosanoids

A

-after you eat linoleic acid (18:2 delta9,12) and a-linolenic acid (18:3 delta9,12,15) are starting points for other polyunsaturated acids (arachidonic acid –> eicosanoid hormones)

42
Q

Palmitate to oleate and everything that comes from the intermediates

A

Palmitate (16:0) —elongation—> stearate (18:0) —desaturation—> Oleate (18:1 delta9)

Palmitate (16:0) can be desaturated to Palmitoleate (16:1 delta9)

Stearate can be elongated to longer saturated fatty acids

43
Q

Linoleate (18:2 delta9,12) to a-linolenate (18:3 delta 9,12,15)

A
  • becomes desaturated and only occurs in plants which is why you need to eat both
  • other polyunsaturated fatty acids can be formed from a-linolenate
44
Q

Linoleate to arachidonate

A

Linoleate (18:2 delta9,12) –desaturation–> gamma-Linolenate –elongation–> eicosatrienoate –desaturation–> arachinoate (20:4 delta5,8,11,14)

45
Q

clinical significance of Stearoyl-CoA desaturase (SCD)

A
  • development of obesity
  • development of insulin resistance that precedes Type 2 diabetes

-synthesis of the SCD1 isoform is induced by dietary saturated fatty acids

46
Q

FA regulation

A

Short-term

  1. Citrate
  2. Acetyl-CoA carboxylase
47
Q

FA regulation: Citrate

A

Citrate signals excess energy to be converted to fat when acetyl-CoA levels are high then it is converted to citrate and its exported to the cytosol

48
Q

FA regulation: Acetyl-CoA carboxylase

A

Catalyzes the rate limiting step

  • inactive when phosphorylated (triggered by glucagon and epinephrine–> when energy is needed)
  • active when dephosphorylated
  • inhibited by end products: palmitoyl-CoA and stearoyl-CoA
  • activated by citrate (citrate is made from acetyl-CoA) but citrate doesnt do much when its already dephosphorylated
  • during FA synthesis production of malonyl-CoA shuts down B-oxidation at level of transport system in mitochondrial inner membrane
49
Q

AMP-dependent protein kinase (AMPK)

A

converts Acetyl-CoA carboxylase to inactive/phosphorylated form

50
Q

protein phosphatase 2A

A

under hormonal control
-removes phosphate from acetyl-CoA carboxylase to activate it

when protein phosphatase 2A is phosphorylated by PKA it is inactivated

51
Q

Major regulation key of fatty acid synthesis and B-oxidation

A

these two will NEVER happen at the same time cause that is futile cycling which is very wasteful

Malonyl-CoA (substrate for FA synthesis) will shut down fatty acid B-oxidation by inhibiting carnitine acyl-transferase I

52
Q

Triglycerides/Triacylglycerols (TG)

A

excess carbs ingested and glycogen stores are full then excess is converted into TG and stored in adipose tissue

-consist of 3 fatty acids esterified through their carboxyl groups to a molecule of glycerol which neutralizes fatty acids and facilitates their storage

53
Q

triacylglycerols and glycerophospholipid synthesis shares what two precursors…?

A
  1. glycerol-3-phosphate (intermediate from glycolysis and initial acceptor of fatty acids during TG synthesis))
  2. fatty acyl-CoA (formed from fatty acids by acyl-CoA synthetases)
54
Q

synthesis of one molecule of triglyceride

A

requires: glycerol-3-phosphate and fatty acyl-CoA

3 Steps

  1. sequential addition of 2 fatty acids from fatty acyl-CoA to form phosphatidic acid
  2. removal of phosphate to form diacylglycerol
  3. addition of a third fatty acyl-CoA to form TG

Insulin promotes this (conversion of carb to TG)!!!!!!
-people with diabetes cant use glucose properly so they cant synthesize fatty acids from carbs or amino acids (if untreated this leads to increased fatty acid oxidation and ketone body formation)

55
Q

effect of glucagon and epinephrine on fatty acids

A
  • release of fatty acids from adipose tissue is stimulated by glucagon and epinephrine
  • decrease rate of glycolysis and increase rate of gluconeogenesis in the liver
56
Q

futile cycling

A

triacylclycerol breakdown and re-synthesis create a futile cycle (tricylglycerol cycle)
-75% of free fatty acids released from lipolysis are re-esterified to form TG rather than be used for fuel (happens in adipose tissue, liver, blood, etc)

may represent an energy treserve in bloodstream during fasting so you can get energy quickly in emergency

MTC Block 2: Post Quiz Material (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions