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BMSC 230 > Mod 8 Bmsc 230 > Flashcards

Mod 8 Bmsc 230 Flashcards

1
Q

B-Oxidation

A

Repetitive process by which fatty acids are broken into acetyl coa in the matrix

  • acetyl coa produced will enter citric acid cycle
  • involves release of NADH and FADH2 (donate electrons to etc - atp generation)
  • B-oxidation cuz B carbon (third from the carboxyl end) gets oxidized every round
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2
Q

Double bonds/ kinks in hydrocarbon chains ___ the melting point of the fatty acid

A

Lower

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3
Q

The last carbon at the methyl carbon end, when numbering from the methyl carbon end

A

Omega (w)

If the double bond is three carbons away from the methyl end, it’s called an omega 3 fatty acid

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4
Q

Fatty acid storage

A

Stored as triacylglycerol, a neutral lipid, in adipose tissue

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5
Q

Adipokines

A

Small biomolecules secreted by adipose tissue that control overall body metabolism and appetite

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6
Q

Triacylglycerol structure

A

Three fatty acids attached to a glycerol backbone via ester bonds

Lipase cleaves the fatty acids off the glycerol and releases them into the blood to be used by other organs —> linked to CoA once in the cell —> undergo beta oxidation in the matrix to release acetyl coA

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7
Q

First stage of fatty acid degradation

A

Mobilization of fatty acids from triacylglycerol in adipose tissue (hydrolysis rxn that uses three water molecules to cleave off three fatty acid residues)

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8
Q

Three lipases and their mechanism

A

Adipose triglyceride lipase (ATGL - triacylglycerol) and Hormone-sensitive lipase (HS-lipase - diacylglycerol)

  • activated by epinephrine and glucagon that signal need for more fuel (bind to receptor on adipose cell and activate camp —> camp activates protein kinase a which activates ATGL and HS lipase)
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9
Q

Fatty acid and glycerol transportation

A
  • Fatty acids bound to the blood protein albumin - go to tissues that need fuel
  • glycerol goes to liver and gets converted to dihydroxyacetone phosphate (can undergo glycolysis or gluconeogenesis) - usually gluconeogenesis
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10
Q

Carnitine

A

Brings fatty acids into mitochondria so they can be oxidized

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11
Q

Second stage of fatty acid degradation

A

Activation of fatty acids and transport to mitochondria

  • fatty acids brought into cell through diffusion through special proteins
  • fatty acids activated by reacting with Coenzyme A to form acyl CoA on the outer mitochondrial membrane (rxn consumes 1 atp and breaks it down into amp and ppi, broken down into two Pi; so 2 high energy bonds are broken for every CoA attached to a fatty acid)
  • acyl of Acyl CoA transferred to biomolecule called carnitine —> formation of acyl carnitine by enzyme carnitine acyltransferase 1 (on cytoplasmic side of the inner mitochondrial membrane)
  • acyl carnitine goes across into mitochondria through a translocase —> carnitine acyltransferase II reverses rxn (reformation of acyl CoA + free carnitine shuttled into cytosol so it can be re-esterified to another fatty acid to bring it into the mitochondria)
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12
Q

Third stage of fatty acid degradation

A

Degradation of fatty Acyl CoA to Acetyl CoA:

  • acyl CoA now in mitochondrial matrix - will undergo beta oxidation
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13
Q

4 reactions in every round of beta oxidation

A

Acyl CoA —> Trans-/_\2- Enoyl CoA —> 3-Hydroxyacyl CoA —> 3-Ketoacyl CoA —> Acyl CoA + Acetyl CoA

  1. Oxidation step producing FADH2: Acyl CoA dehydrogenase (trans double bond produced between a and b carbons due to oxidation)
  2. Hydration step: enoyl CoA hydratase (OH on b and H on a carbon - product is 3-hydroxyacyl CoA)
  3. Oxidation step producing NADH: B-hydroxyacyl CoA dehydrogenase (oxidized to 3-ketoacyl CoA - B Carbon now fully oxidized (C=O))
  4. Thiolysis step: Thiolase (CoA used to cleave off an acetyl CoA unit and leave behind an acyl CoA two carbons shorter - SH attacks bond between a and b) - final round of B oxidation releases two acetyl CoA
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14
Q

Palmitate

A

16-carbon fatty acid yielding 106 ATP upon oxidation

  • requires 7 rounds of B oxidation
  • technically, 108, but two high energy bonds needed to activate the fatty acid to get it into the mitochondria so -2 = 106 vs 30 from glucose

(Don’t confuse with palmitoleate - unsaturated, double bond at carbon 9)

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15
Q

Regulation of fatty acid degradation

A

Synthesis and degradation DONT happen at the same time (reciprocal regulation)

  • epinephrine and glucagon activate triacylglycerol breakdown in adipose but also inhibit the fatty acid synthesis enzyme, acetyl CoA carboxylase
  • carboxylation of acetyl CoA to malonyl CoA necessary for fatty acid synthesis- malonyl CoA inhibits carnitine transferase 1 and therefore b oxidation
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16
Q

Unsaturated fatty acids

A

Double bonds

17
Q

Three stages of fatty acid degradation

A
  1. Mobilization of fatty acids from triacylglycerol in adipose tissue
  2. Activation of fatty acids and transport to mitochondria
  3. Degradation of fatty Acyl CoA to Acetyl CoA
18
Q

Palmitoleate degradation

A

16 carbon fatty acid with a double bond between carbon 9 and 10

  • palmitoleoyl-CoA —> 3 cycles of B oxidation and becomes cis-/\ 3-enoyl CoA (isn’t a substrate for acyl CoA dehydrogenase) —> CIS-/\3-ENOYL COA ISOMERASE (Converts cis double bond between c3 and c4 to trans double bond between c2 and c3) converts to Trans-/_\2- Enoyl CoA- b oxidation can continue
19
Q

Linoleoyl CoA

A

Fatty acid with twO double bonds requiring a reductase

  • 2,4-dienoyl CoA not a substrate for beta oxidation —> reductase reduces the double bond between carbons 4 and 5 using NADPH —> trans-/\3-enoyl CoA converted to trans-/\2-enoyl CoA by cis/_\3 Enoyl CoA isomerase
20
Q

Oxidation of odd chain fatty acids

A

In the last round of beta oxidation, one acetyl CoA and a 3-carbon acyl CoA called propionyl CoA is produced (rather than two acetyl CoA’s)

  • Propionyl CoA gets carboxylated at carbon 3 using atp —> D-methylmalonyl CoA (4c molecule) —> L-methylmalonyl CoA (catalyzed by methylmalonyl CoA mutase, a vitamin B12 containing enzyme) —> Succinyl CoA (can enter CA cycle)
21
Q

Ketone bodies

A

synthesized from acetyl CoA in the liver (instead of going into the citric acid cycle) - water soluble fuel crossing the blood brain barrier (brain- but can be used by kidney and heart). Ketone body production increases when fatty acid oxidation is high:

  • starvation
  • uncontrolled diabetes
22
Q

Three different ketone bodies produced from acetyl CoA in the matrix

A

Acetoacetate, B-hydroxybutarate, acetone

2 acetyl CoA make Acetoacetate —> converted to 3-hydroxybutarate or acetone through SPONTANEOUS decarboxylation (reduce and get rid of co through NADH to make 3hydroxybutarate) — Acetoacetyl CoA was an intermediate

23
Q

Degaradation of ketone bodies

A

3-hydroxybutarate and acetoacetate can be metabolized back to acetyl CoA to be used in the CA cycle - acetone exhaled

  • Liver cannot convert acetoacetate to acetoacetyl CoA so it doesn’t use up the acetoacetate itself (fatty acids are liver’s source of energy)
24
Q

High levels of acetoacetate act on adipose tissue and ____ lipolysis

A

Inhibit

  • by indicating an abundance of acetyl CoA
25
Q

Ketone body degradation process

A
  • dehydrogenase converts 3-hydroxybutarate to acetoacetate
  • CoA transferase coverts acetoacetate to acetoacetyl CoA (succinyl CoA added, succinate leaves)
  • thiolase converts acetoacetyl CoA to 2 acetyl CoA molecules (CoA added)
26
Q

Diabetes

A
  • Insufficient amounts of or response to insulin
  • lack of oxaloacetate
  • high b Oxidation of fatty acids so a large amount of acetyl CoA
  • acetyl coa can’t enter citric acid cycle cuz of lack of oxaloacetate so it’s converted to ketone bodies —> ketoacidosis (ketone bodies are acidic)
27
Q

Insulin

A
  • Increases glucose uptake by the liver
  • metabolism of glucose through glycolysis to pyruvate (some pyruvate converted to oxaloacetate)
28
Q

Fatty acid degradation is aerobic/anaerobic

A

Aerobic

BMSC 230 (9 decks)

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