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Biochemistry 2 > Fatty acid catabolism > Flashcards

Fatty acid catabolism Flashcards

1
Q

How lipids yield energy

A

Through B-oxidation of FA

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2
Q

How liver and heart derive energy

A

80% energy from FA oxidation

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3
Q

What is B-oxidation

A

A four-step enzyme catalyzed process of oxidative removal of 2-carbon units from FA to form acetyl-CoA

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4
Q

Why TGs are the best storage fuels

A

FA chains are highly reduced compounds (mainly single bonds between C and H)
-Yield twice fold energy than CHO and protein
-Insoluble in water- do not increase osmorality( are not bulky for storage)
Relatively inert- no risk of undesirable reactions (can be stored for a long time)

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5
Q

Where lipids are digested ( in what parts of GI)

A

mouth cavity
Duodenum
Stomach

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6
Q

Explain what happens with fats in small intestine and onward

A

1) Bile salts emulsify dietary fats, forming micelles
2) Intestinal lipases degrade triacylglycerols
3) FA and other break down products are taken up by the intestinal mucosa and converted into TGs
4) Tgs are incorporated, with cholesterol and apolipoproteins into chylomicrons
5) Chylomicrons move through the lymphatic system and bloodstream to tissues
6) Lipoprotein lipase, activated by apoC-II in the capillary, converts TGs to FA and glycerol-> uptake

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7
Q

How FA can travel in the body

A

In chylomicrons or NEFAs to albumin

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8
Q

What is going to happen to free FA

A

They are freely absorbed by cells. If cell need energy-> TCA cycle. Not needed-> TGs->storage

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9
Q

Chylomicrons travel through __ and ___, what role does portal system play in it

A

Travel through lymphatic system and circulatory system. Portal system helps to bring all the nutrients to the liver or to other tissues

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10
Q

How chilomicrons are arranged

A

Globular structure.

Tgs and cholesterol inside. The layer is made of apolipoproteins and phospholipids

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11
Q

What is the classification according to the density of lipoproteins

A

VLDL
ILDL(intermediate)
LDL
HDL

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12
Q

How proteins help in release of TGs from chylomicrons

A

When they are stimulated by a ligand they release TGs

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13
Q

Explain how lipid mobilization from storage happen

A

1) glucagon binds to the receptor (GPCR)->cAMP->PKA
2) PKA phosphorylates HSL(enzyme-hormone sensitive lipase) and PKA phosphorylates perilipin.This brings perilipin and HSL at the surface of the lipid droplet.
3) When perilipin is phosphorylated, CGI (comparative gene identification) dissociates ( in this case it is CGI58)
4) CGI-58 moves to ATGL (adipose TG lipase).
5) ATGL becomes active. It attacks TGs and converts it to diacylglycerol+FA
6) HSL does the conversion->monoacylglycerol+FA
7) MGL( monoacylglycerol lipase) converts monoacylglycerol->FA+glycerol

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14
Q

Do FAs travel free in the circulation?

A

No, they are bound to serum albumin

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15
Q

Serum albumin can carry up to ___

A

10 Non-esterified fatty acids (NEFA)

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16
Q

What happens to glycerol after TGs is broken down

A

1) Glycerol is phosphorylated by glycerol kinase with the use of ATP
2) Glycerol 3-phosphate is dehydrogenated by glycerol 3-phosphate dehydrogenase resulting in Dihydroxyacetonephosphate (DHAP)- glycolytic intermediate

3)DHAP is isomerized to D-glyceraldehyde 3-phosphate

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17
Q

Glycerol contributes only __% of the energy from TG

A

5

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18
Q

Fate of FAs when got into the cell - the first step

A

The first step is activation

1) Fatty acyl-Coa synthetase charges FA with ATP resulting in Fatty acyl-adenylate
2) Then Fatty acyl-adenylate can attached to the thiole group of CoA-SH and fatty acyl-CoA synthetase removes AMP resulting in Fatty acyl-CoA

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19
Q

The difference between synthetases and synthases

A

Synthetases- uses ATP

Synthases- do not use ATP

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20
Q

FAs activation is necessary for

A

transportation of FAs into mitochondria for beta-oxidation and for synthesize of longer membrane lipids

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21
Q

Who discovered that enzymes of FA oxidation are located in Mitochondria

A

Kennedy and Lehninger

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22
Q

How activated FAs are transported into mitochondria

A

Small ( less 12C) FA diffuse freely across mitochondrial membranes
-Longer FA are transported with Carnitine transport system

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23
Q

Explain the mechanism of carnitine transport system

A

1) Activated FA-CoA is attached to Carnitine by the enzyme Carnitine acyltransferase I and CoA-SH is removed on the outer membrane
2) Carnitine goes through acyl-carnitine/carnitine -passive transporter transporter in the inner membrane

3) When carnitine gets to the matrix , carnitine acyltransferse II removes carnitine and attaches CoA-SH. Now available for beta-oxidation

24
Q

4 enzymes of beta-oxidation

A

1) acyl-CoA dehydrogenase
2) enoyl-CoA hydratase
3) Beta-hydroxyacyl-CoA dehydrogenase
4) Acyl-CoA acetyltransferase (thiolase)

25
Q

Explain beta-oxidation

A

1) The double bond between the third and the second carbon is created counting from the carboxyl end. The function is performed by acyl-CoA dehydrogenase and use of FAD->FADH2
2) enoyl-CoA hydratase removes double bond and adds OH on the third carbon
3) Beta-hydroxy-acyl-CoA reduces NAD to NADH and thus OH and H on carbon three is turned to only double bond O(carboxyl group)
4) acyl-CoA acyltransferase (thiolase) brings ib CoA-SH and the bond between 2 and 3 carbon is broken down

26
Q

Beta oxidation results in

A

myristoyl-CoA(Acyl-CoA)

Acetyl-CoA

27
Q

Beta-oxidation of 16 FA yields

A

8 acetyl-CoA, 7FADH2, 7NADH,7H+->28ATP and 7H2O

28
Q

How much ATP one FADH2 and NADH yield

A
  1. 5 ATP->FADH2

2. 5->NADH

29
Q

How does beta-oxidation of unsaturated FA happen (If the double bond between carbon 9 and 10)

A

Before carbon 7 everything happens as before.
Now the double bond between carbon 3 and 4

Delta 3, delta 2-enoyl-CoA isomerase transfers the double bond to the carbon 2-3, thus skipping acyl-CoA dehydrogenase

30
Q

What is the result of skipping the first step of beta-oxidation, in unsaturated fat

A

FADH2 is not produced->less energy

31
Q

What if there is two double bonds (at carbon 9 and 10 and 12 and 13) all cis

A

proceeds normally until first double bond is at position 3 and 4 ( two bonds are cis)

Then Delta 3, delta 2-enoyl-CoA isomerase transfers the first bond to carbon 2 and 3 (trans at 2 and cis at 6)

One acetyl-CoA is removed

The next cycle begins

Now we have trans 2 and 3 bond and cis carbon 4 bond. This double bonds at carbon 4 does not allow beta-oxidation to continue.

2,4-dienoyl-CoA reductase comes in and removes this double bond with NADPH.

Now it is trans delta 3 and enoyl-CoA comes and finishes the reaction

32
Q

What FA are more common (numbers)

A

Even number FA are more common; but some plants and marine organisms have odd number FA

33
Q

Explain how beta-oxidation of GA with odd number carbons happen

A

Everything happens fine until last step. There is only 3 carbons left and it is called propionyl-CoA. It is ultimately converted to succinyl-CoA. And coenzyme B12 is important for the conversion

34
Q

What enzymes create energy molecules in beta-oxidation

A

Enzyme 1 and 3 (FADH2 and NADH)

35
Q

Beta-oxidation is regulated by both ___

A

Transcription factors and kinases

36
Q

Where are short and long specific beta-oxidation systems situated?

A

Short-chain in mitochondria floating in the matrix

Very-long-chain-specific -> in the membrane

37
Q

Fatty acyl-Coa synthesized in the cytoplasm is directed to

A

Beta-oxidation or Tg synthesis

38
Q

How beta-oxidation is regulated

A

Malonyl-CoA, the first intermediate of FA synthesis, inhibits Carnitine Acetyltransferase I. ( if cells need more synthesize, degradation is stopped)

  • Low ATP stimulates AMPK leading to activation of CArnitine shuttle
  • High NADH inhibits acyl-CoA dehydrogenase
39
Q

What is omega oxidation

A

Very rare
Only in liver and kidney in endoplasmic reticulum
FA are removed from both ends , yielding acetyl-CoA. This happens faster

40
Q

Why ketone bodies are energy molecules?

A

Because they can be converted back to acetyl-CoA-> TCA cycle

41
Q

Ketone bodies are water/lipid soluble?

A

Water soluble

42
Q

Where ketone bodies are produced

A

in the liver

43
Q

Three types of ketone bodies

A

Acetone
Acetoacetate
D-beta-hedroxybutyrate (BHB)

44
Q

What is the usual concentration of acetone in the body and how it is exceted

A

Low concentration

Excretion-> Exhaled

45
Q

Acetoacetate and BHB are involved in___ and transported to _____

A

Production of acetyl-coA

Transported to other tissues

46
Q

Ketogenesis or ketone bodies synthesis occurs during ___ in___

A

During starvation or diabetes

Occurs in mitochondria within liver

47
Q

What is happening in advanced stages of diabetes

A

A lot of ketone bodies in the liver

Acetone breathe

48
Q

Ketone bodies are generated from

A

Extra acetyl-CoA that is present

49
Q

The first step of ketogenesis

A

2 acetyl-CoA are converted to acetoacetyl-CoA with thiolase (last enzyme of beta-oxidation)

50
Q

The second step of ketogenesis

A

Acetoacetyl-CoA is converted to HMG-CoA with the help of HMG-CoA synthase. This enzyme attaches third acetyl-CoA group

51
Q

Where we can find HMG-CoA synthase

A

In mitochodria and cytoplasm

52
Q

How many acetyl-CoA are sued for generation of ketone bodies

A

Though three are used during the cycle in the third step one is thrown out, so in total only 2 are used

53
Q

What can happen to acetoacetate

A

It can be converted to acetone with acetoacetate decarboxylase or be converted to BDB with BDB dehydrogenase

54
Q

HMG-CoA lyase can be found in

A

Only in mitochondria

55
Q

How ketone bodies catabolism happen

A

Acetoacetate is attacked by beta-ketoacyl-CoA transferase and converts it to acetoacetyl-CoA.

Acetoacetyl-CoA with thiolase is converted to 2 acetyl-CoA

56
Q

What is the particular with the place where you can find beta-ketoacyl-CoA transferase

A

It is absent in the liver. If it was present and it was functional, then ketone bodies would never leave the liver

Biochemistry 2 (17 decks)

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