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BioChemistry > Oxidation Of Fatty Acids and Ketone bodies > Flashcards

Oxidation Of Fatty Acids and Ketone bodies Flashcards

1
Q

Where are fatty acids mainly oxidized

Where are they stored

Why are they oxidized

A
  • heart , liver or kidney
  • stored in adipose tissue

-done during fasting state to produce energy
-during stressful moments ( fight or
Flight )

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2
Q

Types of pancreas cells and what they do

A

-found in islets of langerhans ( cluster of endocrine cells )
1 alpha - secrete glucagon when glucose is gone
2 beta - secrete insulin when glucose is high

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3
Q

How is flight or fight response glucose made

A

-sympathetic nervous system stimulated adrenal medulla cells ( chromafin ) to secrete 80% epinephrine and 20% norepinephrine

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4
Q

What structures surround TRIG’s in adipose cells

A

-perilipin bound to CGI
-ester cleaving enzymes
1 adipose triglyceride lipase
2 hormone sensitive lipase
3 monoglyceride lipase

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5
Q

Describe process from activation of perilipin to cleaving to 1st hormone

A
  • the 3 hormones bind to GPCR on adipocytes, cAMP activates protein kinase A which phosphorylates perilipin bound to CGI
  • CGI dissociates and activates adipose triglyceride lipase
  • ATL cleaved 1st ester bond and 1st FFA released and we are left with diacylglyceride
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6
Q

Describe how middle ester bond is cleaved

And the 3rd

A

-PKA phosphorylates hormone sensitive lipase wc cleaved 2nd ester bond freeing FFA and monoglyceride

/PKA phosphorylates monoglyceride lipase cleaved 3rd ester bond and releases FFA and glycerol

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7
Q

Fate of glycerol and FFA

How are they transported in blood and why

A

-pushed into blood stream to be taken to other cells for oxidation into ATP

  • glycerol diffuses into blood
  • FFA transported by albumin as it aint water soluble
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8
Q

1st step of beta oxidation and why and enzyme involved

Problem of this step ( CoA added )

A

-to prevent fatty acid from leaving cell
-fatty acyl CoA synthetase converts fatty acid into fatty acid acetyl CoA
( ATP dependent )

-fatty acetyl CoA can’t move into mitochondria

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9
Q

Describe transport stage of fatty acids into mitochondria and mediators

A
  • transporter protein ( carnitine acetyl transferase type 1 ) on outer mito membrane removes CoA and adds carnitine
  • product is now fatty acetyl carnitine and can move into Mito via a translocase
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10
Q

Problem of adding carnitine once in mito and solution

A
  • can move out of mito translocase

- remove carnitine and add acetyl CoA back. Enzyme is carnitine Acetyl CoA transferase type 2

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11
Q

What happens to carnitine after being removed

A

-pushed out of Mito into cytosol ti CAT 1 for recycling

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12
Q

Describe 1st step of beta oxidation and mediators

A
  • fatty acetyl CoA is oxidized by acetyl CoA dehydrogenase
  • FAD reduced to FADH2
  • double bond formed between alpha and beta carbon atoms
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13
Q

Describe 2nd step of beta oxidation and mediators

A
  • H20 added across trans double bond ( trans delta 2 Enol CoA ) and alpha and beta by enzyme Enol CoA transferase
  • product beta hydroxyl acetyl CoA
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14
Q

Describe 3rd step of beta oxidation and mediators

A

-beta hydroxyl acetyl CoA has its 2 hydrides removed at beta and a double bond between C and Oxygen forming beta ketoacyl CoA
/enzyme is beta ketoacyl dehydrogenase

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15
Q

Describe what happens at 4th step of beta oxidation and mediators

A
  • beta ketoacyl CoA cleaved at Alpha and beta bond to form acetyl CoA ( krebbs cycle ) and a fatty acyl CoA recycled at 1st step of beta oxidation but 2 carbons short
  • enzyme is thiolase
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16
Q

How to calculate number of acetyl CoA’s and rounds of oxidation of a even number fatty acid

A
  • divide by 2 for number of acetyl CoA made

- less one of acetyl CoA for Cycles of beta oxidation

17
Q

What are the 2 products of beta oxidation of odd chain fatty acids and fates of the products

A
  • acetyl CoA ( krebbs cycle )

- propionly CoA ( 3 carbon molecule ) converted to succinyl CoA

18
Q

1st step in converting propionly CoA into succinly CoA and mediators

And 2nd step

A
  • C atom form HCO3 or CO2 added to propionly CoA
  • Enzyme is propionly CoA carboxylase ( biotin dependent )

-methyl malonyl CoA mutase enzyme ( B12 ) dependent converts methyl Malonyl CoA into succinly CoA

19
Q

What does deficiency of B12 cause

List the fates of succinly CoA

A
  • perinicious anemia
  • fatigue
  • converted into succinate ( krebb cycle intermediate )
  • converted into OAA then Malate ( gluconeogenesis )
  • converted into poryphyrin and heme group used to make erythrocytes
20
Q

Describe oxidation of fats inside peroxisomes

A
  • has transporters to take in fatty acetyl CoA which is oxidized by FAD
  • but FADH2 hydrides taken and given to o2 and H2O to form peroxide which has numerous cellular functions
21
Q

How does the body prevent excess peroxide’s

A

-catalyse enzyme breaks down peroxide into water and oxygen

22
Q

Describe oxidation of odd chain fatty acids

A
  • eg polmitoleate activated and moved into Mito matrix
  • goes 3 cycles of beta oxidation , 3 acetyl CoA released until It is now delta 3 Enol CoA
  • enzyme cis delta 3 Enol CoA isomerase converts delta 3 Enol CoA into trans delta 2 Enol CoA
  • beta oxidation continues
23
Q

Why can’t step 1 enzyme of beta oxidation act on cis delta 3 Enol CoA

A

-it adds a double bond to alpha and beta carbons but in this case double bond already present between beta and 4th carbon

24
Q

Describe oxidation of even numbered unsaturated fatty acid

( linoleate example ) 18:2 delta 9,12

A

-activate and translocated into Mito matrix
/undergoes 3 cycles of beta oxidation and reduced to 12 carbon fatty acid ( cis delta 3 Enol CoA )
/enzyme cis delta 3 Enol CoA isomerase converts it into trans delta 2 Enol CoA which undergoes beta oxidation
/now we form cis delta 4 Enol CoA
-undergoes 1st step by acetyl CoA dehydrogenase forming 2,4 dienol CoA intermediate wc isn’t compatible with hydratase
-2,4 dienol CoA reductase removes double bonds and adds one at carbon 3 and 4
-isomerase shifts it to alpha and beta carbons
-beta oxidation continues

25
Q

When are ketone bodies utilized as an energy source

A

1 hypoglycemia
2 prolonged starvation
3 low carbohydrate diet
4 diabetes mellitus

26
Q

Where are ketone bodies made and where are they mainly utilized

A
  • made in the liver ( main site of fat oxidation )

- heart , brain and muscle

27
Q

What happens when there is low glucose in the body ( to OAA , glucose and acetyl CoA )

A
  • increased beta oxidation of fats
  • increased ATP , acetyl CoA and NADH
  • oxaloacetate converted into glucose via gluconeogenesis and less OAA means acetyl CoA can’t fuse with it to form citrate
  • acetyl CoA now In excess and undergoes ketogenesis
28
Q

Describe 1st step of ketogenesis and mediators

A
  • 2 acetyl CoA’s fuse and there is loss of a CoA
  • we form aceto acetyl CoA
  • Enzyme is acetyl CoA acyl transferase
29
Q

Describe 2nd step of ketogenesis

And it’s defining reaction characteristics

A
  • aceto acetyl CoA has another acetyl CoA added and a CoA is removed
  • we form HMG CoA ( 3 hydroxy 3 methy glyceterol CoA )
  • Enzyme is HMG CoA synthetase

-rate determining step

30
Q

What happens to HMG CoA after formed and mediators

A

-HMG CoA lyase enzyme removes a acetyl CoA to form acetoacetate ( 1st ketone body )

31
Q

2 reactions that can occur to acetoacetate

A

1 NADH drops hydrides on it to form beta hydroxybutyrate ( 2nd ketone body )
-enzyme is beta hydroxybutyrate dehydrogenase

2 decarboxylated by CO2 removal and enzyme acetoacetate decarboxylase ( removes a C atom ) to form acetone

32
Q

What occurs to the breath of diabetic people and describe how it come about

A

-diabetic mellitus patience undergo numerous ketone metabolism , produce a lot of acetone which the body tries to exhale giving breath a fruity smell

33
Q

What is ketonemia and ketonuria

What is the normal ketone bodies conc

Which 2 ketone bodies are used as energy sources

A
  • excess of ketone bodies in blood
  • in urine
  • 0.2 mmol/ L
  • acetoacetate and beta hydroxybutyrate
34
Q

We do ketone bodies do at the brain stem

A

/they stimulate the brain stem at the area of postremia ( chemotrigger zone )which triggers vomiting
-excessive and loss salts and fluids
-low blood pressure due to hypovolemia ( liquid portion of plasma is low )
Comatose state

35
Q

Dangers of ketone bodies in the blood

A

-they are acidic , ( donate protons in plasma ) making it acidic , or ketoacidosis

  • Bohr effect
  • chromatin clumping
36
Q

Describe how the body fights against

A

1 bicarbonate carbonic acid buffer tries but only for a few seconds
2 hyperventilate to reduce CO2 and reduce carbonic acid formation ( kossmal breathing - rapid deep inspirations )

37
Q

Describe how ketone bodies are utilized as energy source

A

1 beta hydroxybutyrate dehydrogenase collects hydrides from beta hydroxybutyrate and converts it into acetoacetate ( other acetoacetate from blood )

2 enzyme thiophorase transfers CoA from succinly CoA and transfers to acetoacetate and forms aceto acetyl CoA

3 enzyme acetyl CoA acyl transferase adds another CoA and cleaves aceto acetyl CoA into 2 acetyl CoA. Which are used in krebbs cycle

38
Q

What doesn’t the brain use FA direct

A

/can’t diffuse Through the blood brain barrier

BioChemistry (15 decks)

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