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NUTR 301 > Lipids 4: Fatty Acid Metabolism I > Flashcards

Lipids 4: Fatty Acid Metabolism I Flashcards

1
Q

What does fat metabolism depend on?

A

glucose status

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2
Q

What is the general change in plasma levels of fuels after consumption of a meal?

A
  • TG: goes up slowly, more work for TG to get from diet into circulation, also does not go up much
  • FFA: go down when we eat, controlled more so by what is coming out of the adipose tissue so more used in fasting
  • ketone bodies: nothing really happens, usual only applicable in longer fasting
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3
Q

What are the tissue specific metabolism of the brain?
* fuels used
* fuels released

Know this!

A
  • fuels used: glucose, ketone bodies, lactate (when [plasma] elevated)
  • fuels released: lactate
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4
Q

What are the tissue specific metabolism of the skeletal muscle?
* fuels used
* fuels released

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A

Power house of the body so it gets fuel from a bunch of different sources
* fuels used: glucose, FFAs, TGs, branched chain AA, lactate
* fuels released: lactate, alanine glutamine

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5
Q

What are the tissue specific metabolism of the heart?
* fuels used
* fuels released

Know this!

A
  • fuels used: FFAs, TGs, ketone bodies, glucose, lactate
  • fuels released: NA
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6
Q

What are the tissue specific metabolism of the liver?
* fuels used
* fuels released

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A

Uses everything especially since it is a controller
* fuels used: AAs (partial oxidation), FFAs, lactate, glycerol, glucose, alcohol
* fuels released: glucose, ketone bodies, lactate (during absorptive phase), TGs

Also site of galactose and fructose metabolism

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7
Q

What are the tissue specific metabolism of the intestine?
* fuels used
* fuels released

Know this!

A
  • fuels used: glucose, glutamine
  • fuels released: lactate, alanine

Also releases dietary glucose, galactose, fructose, AAs & lipids

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8
Q

What are the tissue specific metabolism of the RBCs?
* fuels used
* fuels released

Know this!

A
  • fuels used: glucose
  • fuels released: lactate
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9
Q

What are the tissue specific metabolism of the kidney?
* fuels used
* fuels released

Know this!

A
  • fuels used: glucose, FFAs, ketone bodies, lactate, glutamine
  • fuels released: glucose (renal gluconeogenesis important in prolonged starvation)
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10
Q

What are the tissue specific metabolism of the adipose tissue?
* fuels used
* fuels released

Know this!

A
  • fuels used: glucose, TGs
  • fuels released: glycerol, FFAs, lactate
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11
Q

What determines the fate of Acetyl-CoA?

A

An individuals energy state

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12
Q

What is the overall route of glucose in the fed state regarding FA & lipid metabolism?

A

Net flux of orange outline
* Glucose comes into the liver and makes pyruvate in the cytosol which pyruvate enters mito and becomes AcetylCoA. AcetylCoA can go into a few different places but when the liver does not need all this energy in the fed state the AcetylCoA will be converted to fatty acids.

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13
Q

How does synthesis of long chain fatty acids occur?

A
  • de novo lipogenesis (DNL)
  • modifications of exogenous FAs
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14
Q

What determines the rate of DNL?

A

Regulated a lot by insulin
* genetics, obesity, diet, fed/fasting state, energy state of individual
* DNL is increased in insulin resistance, fatty liver disease, CHO induced hypertryglyceredemia (HTG), and fed state

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15
Q

How much can the rate of DNL differ between people?

A

<5%-35%
* Most healthy individuals have a low rate of DNL where <5% of FAs transported from the liver are de novo, but can be up to 35% in some individuals

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16
Q

What is the site of fatty acid synthesis?

A
  • major site is in the liver hepatocytes cytosol
  • also occurs in adipose
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17
Q

What is AcetylCoA converted to in FA synthesis?

A

Acetyl-CoA → Palmitate

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18
Q

What is the first committed step and enzyme of FA synthesis? what regulates the enzyme?

A

The conversion of Acetyl CoA → Malonyl CoA which is determined by the RLS enzyme Acetyl CoA Carboxylase (ACC)
* activated by insulin (insulin-dependant dephosphorylation)
* activated by citrate build up
* inhibited by palmitate build up
* inhibited by cAMP-dependant phosphorylation

19
Q

Where in the cell can Acetyl-CoA be generated?

A
  • mito matrix
  • cell cytosol
20
Q

Where does Acetyl-CoA in the mito come from? In which state will the sources be more active?

A

2 sources:
* PDH complex during fed state
* FA oxidation during fasting state

21
Q

Where does Acetyl-CoA in the cytosol come from?
In which state does Acetyl-CoA show up in the cytosol?

A

Glucose goes into the cytosol and is converted to pyruvate which goes into the mito and becomes Acetyl-CoA via PDH. Acetyl-CoA is converted to citrate in the mito which builds up and then leaves the mito into the cytosol where it continues to build up. Citrate built up in the cytosol is converted to Acetyl-CoA (cytosilic) which then goes into FA synthesis.
* More active during fed state

22
Q

How does FA synthesis regulate fatty acid oxidation?

A

Oxidation is reciprocally regulated
* The Malonyl CoA produced during FA synthesis inhibits the enzyme carnitine palmitoyltransferase (CPT1) which breaks down fats

23
Q

How do insulin and glucagon regulate FA synthesis?

A
  • high blood glucose will increase insulin release (decrease glucagon). Insulin stimulates phosphatase which dephosphorylates ACC activating it to convert Acetyl-CoA to Malonyl-CoA
  • low blood glucose will increase glucagon release (decrease insulin). glucagon stimulates PKA which phosphorylates ACC inhibiting it and preventing FA synthesis.
24
Q

How does citrate and palmitate regulate FA synthesis?

A

Citrate is a ‘feed-forward’ activator for ACC and thus FA synthesis
* fed state: ↑ citrate in mito + ↓ cytosilic long-chain acyl CoA → ↑FA synthesis
* fasting state: opposite so negative feedback regulation whereby build up of palmitoyal CoA will inhibit ACC and thus FA synthesis

25
Q

What are the main FAs that get made from FA synthesis?

A
  • palmitate 16:0 (major)
  • stearate 18:0
  • palmitoleate 16:1(n-7)
  • oleate 18:1
26
Q

What is the second and final committed step of of FA synthesis?

A

Chain elongation in the smooth ER by 2 C’s so the growing chain produced even # FAs via the FAS enzyme, fatty acid synthase

27
Q

What happens in one cycle of elongation during FA synthesis?

A

The addition of 2 Cs are reduced, dehydrated, reduced again allowing the next 2 Cs to be added via FAS

28
Q

Regulation of FAS enzyme

A

regulated mostly at level of protein/gene (not allosteric or phosphorylation) - transcriptional & translational SREBP-1c
* Fed state ↑ FAS expression
* fasted state ↓ FAS expression
* CHO feeding ↑ FAS via upregulation of SREBP-1c & ChREBP
* PUFAs ↓ FAS expression

29
Q

FAS to make SFAs, MUFAs, MUFAs

A
  • SFAs: Greater elongation of 16:0 occurs (18:0…), but not well understood and happens differently in various organs & cells but enzyme activity similar to FAS
  • MUFAs: delta-9 desaturase initiates desaturation reaction (14:1. 16:1, 18:1…)
  • PUFAs: multiple desaturation & elongation steps but double bonds cannot be introduced after delta-9 position (n ω-3 or ω-6 bonds can be added)
30
Q

Why is FA composition important?

A

The chain length and degree of saturation influences membrane functions, cell signaling, and has health implications

31
Q

FA composition of adipose tissue

A

shows ~1⁄2 is oleate (18:1) & 1⁄4 is palmitate (16:0) and is a combination of 3 sources of FAs:
1. dietary source (exogenous),
2. dietary FAs that have been elongated &/or desaturated
3. de novo synthesized fatty acids (endogenous)

32
Q

How do we store FFAs?

A

TG is the storage form because FFAs can act as a detergent
* form micelles in solution and acts as detergents in the presence of lipid membranes.

33
Q

Where must the cell obtain FAs to make TGs?

A
  • De novo synthesis
  • FAs taken up from circulation as FFAs (from lypolysis or lipoproteins)
34
Q

How are FFAs present in circulation to be taken up cells?

A
  • Released by lipolysis of adipose tissue & associated with plasma albumin during fasting
  • Generated locally from circulating lipoproteins, by the action of lipoprotein lipases localized on the endothelium of the capillaries within the tissue
35
Q

What makes up a TG?

A

3 Fatty acyl-CoAs + Glycerol 3-P

36
Q

Basic steps of FAs being converted to TG?

A
  1. FAs taken up by cell by passive difussion or FA transporters
  2. FAs transported within the cell bound to FA binding proteins (FABPs)
  3. Re-esterification of FAs into TGs via acyltransferase which happens on surface of ER and gain access to ER once reformed
37
Q

What are the transporters on cells that take up FAs for TG synthesis?

A
  • Fatty acid translocase (FAT/CD36)
  • Fatty acid transport proteins (FATPs)
  • Plasma membrane fatty acid binding protein (FABPpm)
38
Q

What are the 2 pathways for TG biosynthesis?

A
  • Monoacylglycerol pathway (major in enterocytes)
  • Glycerol 3-phosphate pathway (enterocytes & other tissues)
39
Q

Monoacylglycerol pathway for TG biosynthesis

A
40
Q

Glycerol 3-phosphate pathway for TG biosynthesis

A
41
Q

Where does TG synthesis occur?

A

All tissues that store TG

42
Q

Where does TG synthesis occur?

A

All tissues that store TG

43
Q

Why is fructose lipogenic?

A

Hepatic fructose metabolism begins with phosphorylation by fructokinase . Fructose carbon enters the glycolytic pathway at the triose phosphate level (dihydroxyacetone phosphate & glyceraldehyde-3- phosphate). Thus, fructose bypasses the major control point by which glucose carbon enters glycolysis (phosphofructokinase), where glucose metabolism is limited by feedback inhibition by citrate & ATP. This allows fructose to serve as an unregulated source of both glycerol- 3-phosphate & acetyl- CoA for hepatic lipogenesis.
P, phosphate.

44
Q

Sources of fatty acids

A

NUTR 301 (32 decks)

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