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MCG > SYLLABUS 8: Fatty acid oxidation & ketone body production > Flashcards

SYLLABUS 8: Fatty acid oxidation & ketone body production Flashcards

1
Q

what does oxidation of fatty acids provide

A

9 Kcal/g of energy

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2
Q

where are fatty acids important

A

major source of energy for most tissues; but not RBC or BRAIN

major storage form of energy, as triglycerides

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3
Q

where does out dietary fat come from

A

triglycerides, 3 fatty-acid esters of teh alcohol, glycerol

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4
Q

general chemical structore of a fatty acid?

A

CH3 - (CH2)n - COOH

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5
Q

structure of triglycerides?

A

glycerol backbone

3 fatty-acids in ester linkage

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6
Q

size of most fatty acids in our diet?

A

16 to 18 carbons

some contain double bonds in methylenes = unsaturated fatty acids - i.e. oleic acid

if >1 double bond, = polyunsaturated fatty acids, i.e. linoleic acid

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7
Q

what are fatty acids synthesized from

A

acetyl CoA

which came from pyruvate, which came from glucose

requires lots of energy to make fatty acids - NADPH - from pentose cycle, shuttles

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8
Q

what is the function of lipases in our diet?

what organs produce lipase?

what organs are involved w/ its action?

A

pancreas produces lipase;

lipase hydrolyzes dietary triglycerides to fatty acids + glycerol

bile salts from liver aid this

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9
Q

function of adipose tissue re: triglycerides?

A

fatty acids and glycerol are taken up by adipose tissue

triglycerides are resynthesized and stored largely in adipose tissue

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10
Q

functions of fatty acids?

A
  1. component of phospholipids & glycolipids of biological membranes
  2. major energy source for most tissues
  3. major storage form of energy as triglycerides
  4. produce signal transduction molecules, eg inositol phosphates, diacylglycerol
  5. produce prostaglandins and leukotrienes
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11
Q

when are fatty acids the main fuel for tissues?

A

in the fasted state

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12
Q

what activates or inactivates lipase? result re: fatty acids?

A

in the FASTED STATE: glucagon, epinephrine, norepinephrine activate lipase via cAMP-dependent PKA phosphorylation

in the FED STATE: insulin inhibits lipase by dephosphorylation

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13
Q

where does fatty acid oxidation take place?

A

mito & some peroxisomes

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14
Q

describe process of Fatty Acid oxidation in Mito and Peroxisomes, before B-oxidation

A
  1. glucagon, epi, or norepi activate the hormone-sensitive lipase by cAMP-dependent PKA phosphorylation
  2. activate lipase hydrolyses stored triglycerides to glycerol + fatty acids
  3. glycerol exits adipose tissue, goes to liver, enters gluconeogenesis or glycolysis at G3P & DHAP level
  4. fatty acids also can bind albumin in blood, transport to tissues; but albumin-fatty acid complex can’t cross blood brain barriers, so fatty acids do not reach brain for oxidation
  5. fatty acids are transported from albumin to fatty acid binding proteins for delivery inside the tissue
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15
Q

pathway of fatty acid oxidation?

A

B-oxidation pathway

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16
Q

once fatty acid is in the cell, how does it get into the inner mito membrane?

A
  1. fatty acid is brought to cell membrane by fatty acid binding protein
  2. fatty acid is activated to the fatty acyl CoA ester by acyl CoA synthase

this involves exchange of ATP + CoA for AMP + Pi

if short or medium chain acyl CoA synthase, fatty acid can directly enter the mito

if long, need a carnitine shuttle to enter

  1. carnitine shuttle converts long-chain fatty acyl CoA to long-chain fatty acyl carnitine
  2. long-chain fatty acyl carnitine enters the mito via carnitine translocase carrier
  3. in mito, fatty acyl carnitine interacts w/ carnitine transferase 1 or 2 to regenerate carnitine & fatty acyl CoA
  4. fatty acyl CoA undergoes B-oxidation

carnitine is shuttled out of matrix by carnitine translocase carrier, so it can do more carries of fatty acyl CoA into mito matrix

17
Q

what fatty acids need carnitine shuttle? fxn?

A

brings fatty acids from long chain fatty acyl CoA synthases (>12 C) into the inner mito matrix

short or medium chain (4-8 C or 8-12 C) do not need carnitine shuttle

18
Q

what is B-oxidation? products of it?

A

a series of 4 enzyme catalyzed reactions that acyl CoA undergoes

splits a 2C fragment of the acyl CoA to produce acetyl CoA + new fatty acyl CoA shortened by 2 C atoms

reaction produces 1 NADH and 1 FADH2 in steps 1 and 3 of the rxn

19
Q

how long does the B-oxidation process continue for?

A

it’s a spiral, repeats until all the carbons are oxidized to acetyl CoA

each spiral produces 1 FADH2 and 1 NADH

20
Q

how many times would an 18 C fatty acid undergo B oxidation?

products?

A

8 spirals

this produces 8 NADH, 8 FADH2, and 9 2C acetyl CoA products

21
Q

how are odd chain fatty acids differently oxidized in B oxidation?

A

products are acetyl CoA (2C product) and propionyl CoA (3C product)

propionyl CoA undergoes 3 step metabolism reaction to become succinyl CoA

  1. propionyl CoA acted on by biotin produces D-Methyl malonyl CoA
  2. MMA epimerase acts on D-MM CoA, produces L-MM CoA
  3. MMA mutase, using B12, acts on L-MM CoA, produces succinyl CoA
22
Q

what regulates the rate of B-oxidation?

A

1) availability of fatty acids via activated hormone-sensitive lipase
2) availability of **carnitine **
3) **malonyl CoA **is the rate-limiting step of fatty acid synthesis, inhibts carnitine acyl transferases 1 and 2
4) rate of the electron transport chain

23
Q

what controls the availability of carnitine?

A

1) inborn errors of metabolism which lower carnitine synthesis
2) lysine synthesizes carnitine in mammals

24
Q

how many ATPs are produced by B-oxidation of a C18 fatty acid?

A

8 NADH -> 20 ATP

8 FADH2 -> 12 ATP

9 acetyl CoA -> 90 ATP

  • 2 ATP used to activate the fatty acid

= net ~120 ATP prouced

25
Q

what happens to acetyl CoA if the TCA cycle isn’t functioning?

i.e. if OAA is depleted by gluconeogenesis?

A

it cannot enter the TCA cycle

do not want this acetyl CoA to pile up, as this would deplete CoASH and fatty acid oxidation wouldn’t continue

**liver (and small extent kidneys) do ketone bodies formation / ketogenesis to metabolize actyl CoA **

26
Q

when isn’t OAA available

A

gluconeogenic conditions, since then OAA is pulled out of the mito to make glucose

27
Q

where does ketogenesis occur

A

the liver mitochondria

28
Q

describe the process of ketogenesis?

A

overall, 2 acetyl CoAs are converted to acetoacetate

occurs in the mitochondria

  1. acetyal CoAs -> acetoacetyl CoA, by thiolase
  2. acetoacetyl CoA -> HMG COA, by HMGCoA synthase
  3. HMGCoA -> Acetoacetate + Acetyl CoA, by HMGCoA lyase
  4. **Acetoacetate **-> B-OH butarate or -> acetone + CO2 (by spontaneous decarboxylation)
29
Q

on whom is acetone detectable? why?

A

breath of diabetics, fasting individuals, alcoholics

because acetoacetate is produced from ketogenesis, and this spontaneously decarboxylates to acetone + CO2; an spell acetone on these ppl

30
Q

what happens to the products of ketogenesis?

A

they leave the mito of the liver on carrier 5; leave the liver; go to the blood; go to different tissues, where they’re converted back to acetyl CoA, oxidized in the TCA cycle

31
Q

effect of high levels of ketone bodies in the blood?

A

= ketosis

ketone bodies are strong aids

alter (lower) blood pH greatly

32
Q

who has ketosis?

A

diabetics, poorly nourished alcoholics

33
Q

where do ketone bodies made in liver supply energy to?

A

othe rtissues

esp muscle, heart, kidney cortex

34
Q

does brain oxidize ketone bodies?

when/if?

A

no

because the transferase that converts acetoacetate to acetoacetyl CoA isn’t present in the brain

ONLY under conditions of stress i.e. starvation, which allows brain to oxidize ketone bodies, use them for fuel - lowers brain’s need for glucose utilization

35
Q

what happens to the products of ketogenesis?

A

are converted to acetyl CoA which circulates in blood, goes to other tissues, undergoes teh TCA cycle and makes energy

36
Q

what is the peroxisomal fatty acid system?

A

makes some acetyl CoA

preferentially oxidized very long chain fatty acids of C22-26, to median chains, which will go to the mito, where they’re oxidized

produces acetyl CoA and NADH, NO FADH2 - instead, O2 is used as an e- acceptor, producing H2O2 which **peroxisomal catalse **removes

37
Q

how do the products of peroxisomal fatty acid oxidation enter the mito?

A

1) acetyl CoA enters the mito as acetyl carnitine, where it’s oxidized in the TCA cycle
2) NADH is transported into mito by malate-aspartate shuttle
3) spiraling continues til medium chain fatty acid’s produced, which enters mito B-oxidation pathway

38
Q

what induces the peroxisomal fatty acid oxidation pathway?

A

clofibrate and fibrates, drugs that are used to lower serum lipid levels by enhancing peroxisomal fatty acid oxidation

MCG (77 decks)

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