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U6 MCP > Fatty Acid Storage, Mobilization, and Oxidation - CB > Flashcards

Fatty Acid Storage, Mobilization, and Oxidation - CB Flashcards

1
Q

what enzyme do adipocytes release in response to insulin?

A

lipoprotein lipase

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2
Q

Insulin promotes the uptake of what 2 molecule in adipocytes?

A

fatty acids and glucose

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3
Q

Once released from adipocytes, lipoprotein lipase binds to what cells?

A

Endothelial

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4
Q

What transporter move glucose into adipocytes

A

GLUT4

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5
Q

What enzyme is inhibited by insulin?

A

hormone sensitive lipase: stops the breakdown of stored TGs

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6
Q

What is the protein NEFAs are bound to in adipocytes?

A

ALBP (adipocyte lipid binding protein)

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7
Q

What enzyme in adipocytes converts NEFAs to Fatty acyl CoA?

A

Thiokinase or acyl-coa synthase (much easier name)

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8
Q

Is there a transporter needed for NEFAs to get into adipocytes?

A

Yes, FA transporter (FATP1)

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9
Q

What are the substrates for fat storage? What is the enzyme needed?

A

glycerol 3P and Fatty-acyl Coa, acyl transferases

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10
Q

What is the product after the first two FAs are transferred to the glycerol 3P in FA storage? What must happen before the third FA is added?

A

phosphatidic acid, the phosphate must be removed from carbon 3 of yeilding diacylglycerol. The third FA can now be added.

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11
Q

What type of bonds connect FAs to glycerol?

A

Ester

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12
Q

What is lipolysis?

A

Exactly what is seems like. The breakdown of triglycerides into glycerol and NEFAs. esterases do this

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13
Q

What activates hormone sensitive lipase?

A

glucagon and catecholamine

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14
Q

What cells is hormone sensitive lipase found?

A

adipose and steroid hormone producing cells

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15
Q

Is hormone sensitive lipase the rate limiting step of TG breakdown?

A

No, there are other enzymes like adipose triglyceride lipase

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16
Q

Is adipose triglyceride lipase hormone sensitive?

A

No

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17
Q

What does adipose triglyceride lipase do?

A

The first step of TG breakdown. ie the removal of the first FA chain (TG-> DG + 1 NEFA)

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18
Q

Is adipose triglyceride lipase tissue specific or broadly distributed?

A

In many tissue types

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19
Q

Hormone sensitive lipase is ________(active or inactive) when phosphorylated?

A

active

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20
Q

What affect does increased cAMP have on Hormone sensitive lipase?

A

Activates it (Phosphorylates it by cAMP-dependent kinase)

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21
Q

Hormone sensitive lipase is feedback inhibited by what?

A

NEFAs (may not be clinically significant because NEFAs are quickly shuttled away by ALBP to be unloaded into the blood where they bind to albumin)

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22
Q

What is perilipin? How is it regulated?

A

A protein in adipocytes what blocks the breakdown of TGs (unphosphorylated). Once phosphorylated, the perilipin no longer blocks the TGs and allows for lipolysis.

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23
Q

Which fat droplets are metabolically active, the large central droplet or the small peripheral droplets?

A

peripheral

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24
Q

What protein helps Hormone sensitive lipase dock onto a peripheral fat droplet?

A

lipotransin

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25
Q

How are NEFAs transported in the blood? (Free or bound) if bound to what protein?

A

bound to albumin

26
Q

How does gylcerol from lipolysis leave the adipocyte

A

AQPad transporter

27
Q

What carbon does the delta naming system start with?

A

carbonyl carbon

28
Q

What carbon does the omega naming system start with?

A

methyl end carbon

29
Q

What Fatty acids are essential? Why?

A

linoleic and linolenic, polyunsaturated omega-6 and omega-3 FAs cannot me synthesized in mammals

30
Q

Where does beta-oxidation take place?

A

mitochondria

31
Q

Beta OX: What is fatty acid activation? What enzyme is used? is it ATP dependent?

A

addition of a CoA to an FA resulting in acyl-CoA, acyl-CoA synthetase (thiokinase), yes it uses 2 ATP per FA activated

32
Q

Beta OX: the FA is transfered from fatty acyl-CoA to what molecule? What enzyme does this?

A

carnitine yielding acyl-carnitine, carnitine palmitoyl transferase 1

33
Q

Beta OX: What molecule is transported into the mitochondrial matrix and by what transpoter? (the transporter is on the inner Mito membrane)

A

acyl-carnitine,

34
Q

Beta OX: once inside the matrix, acyl-carnitine is converted to what? By what enzyme?

A

acyl-CoA, carnitine palmitoyl transferase 2

35
Q

Beta OX: Where is carnitine palmitoyl transferase 1 (CPT1) found? CPT2?

A

outer mitochondrial membrane, inner

36
Q

Beta OX: What is the first major control point of Beta oxidation?

A

entry into the mitochondria

37
Q

Beta OX: What is carnitine palmitoyl transferase 1 inhibited by?

A

malonyl-CoA (product of first committed step of beta ox). This keeps acyl-CoA out of the mitochondria

38
Q

Beta OX: Fill in the enzymes: (4)
acyl-CoA________> delta2 trans Enoyl-CoA_______> L-3-hydroxy acyl-CoA________> 3-keto acyl-CoA_______> acetyl-CoA + 2 carbon shorter acyl-CoA

A

acyl-CoA dehydrogenase, delta2 enoyl-CoA hydratase, L-3-hydroxy acyl-CoA dehydrogenase, thiolase

enzymes 2-4 are all in a trifunctional enzyme

39
Q

Beta OX: What enzymes in beta oxidation require cofactors

A

acyl-CoA dehydrogenase (FAD yields FADH2), L-3-hydroxy acyl-CoA dehydrogenase (NAD yields NADH), thiolase (CoA-SH)

40
Q

Fact: mitochondria contain 3 distint acyl-CoA dehydrogenases specific to long, medium, and short chain FAs

A

Throw something at Ryan if he’s within sight`

41
Q

list the steps of beta oxidation and reaction type

A
  1. formation of a trans double bond by acyl-CoA dehydrogenase yielding FADH2
  2. hydration of the double bond by delta2 enoyl-CoA hydratase
  3. dehydrogenation yielding NADH2 by L-3-hydroxy acyl-CoA dehydrogenase
  4. thiolysis giving acetyl-CoA + 2 carbon shorter acyl-CoA by thiolase

acyl-CoA_1> delta2 trans Enoyl-CoA_2> L-3-hydroxy acyl-CoA_3> 3-keto acyl-CoA_4> acetyl-CoA + 2 carbon shorter acyl-CoA

42
Q

Beta OX: Fact: LCHAD (long chain hydroxyacyl-CoA dehydrogenase) deficiency exists.

A

eat

43
Q

Beta OX: medium chain acyl CoA dehydrogenase deficiency: Sorry no question

A

fatal if not detected, build up of octanoylcarnotine, treated by avoiding fasting, fat restricted diet. most common mutation (90%): K304E

44
Q

Beta OX: energetics formula: This is how I think of it, it may help it may confuse the shit out of you….

X= # of Carbons in the FA/2
FA= X acetyl-CoAs + (X-1) FADH2s + (X-1) NADHs

1 acetyl coa= 1 GTP(or ATP) + 3 NADH + 1 FADH2
1 NADH= 3 ATP
1 FADH2= 2 ATP

So…
total ATP = X(1 ATP) + X(9 ATP) + X(2 ATP) + (X-1)(3 ATP) + (X-1)(2 ATP)

or more simplified and the way i remember it…

total ATP= X(12 ATP)+ (X-1)(5 ATP)

remember to subtract 2 ATP for fatty acid activation to get the FA into the mitochondria

so. ..
* Net ATP= X(12 ATP)+ (X-1)(5 ATP) - 2 ATP*

A

X= # of Carbons in the FA/2

total ATP= X(12 ATP)+ (X-1)(5 ATP)

remember to subtract 2 ATP for fatty acid activation to get the FA into the mitchondria

so. ..
* Net ATP= X(12 ATP)+ (X-1)(5 ATP) - 2 ATP*

example:

16 Carbon FA:
X = 16/2 = 8

total ATP= (8x12) + (7x5) = 131

net ATP+ (8x12) + (7x5) - 2 = 129

easy right?

45
Q

Beta OX: how may ATP per carbon oxidized in Beta ox?how may ATP per carbon oxidized in gylcolysis?

A

8 ATP/ carbon, 6 ATP/ carbon

46
Q

Beta OX: What causes the issues when trying to break down unsaturated FAs? What enzyme overcomes this? Is there an ATP cost?

A

beta,gamma (cis3) double bond and delta4 double bond,

the cis3 is converted to the normal trans2 double bond via enoyl-CoA isomerase, and beta ox proceeds as normal

The delta4 double bond must be reduced by NADPH dependent reductase to the trans3 double bond then enoyl-CoA isomerase changes it to the normal trans 2 double bond

COST: 1 NADPH for the delta 4 double bonds
1 FADH2 for cis3 double bonds (dont need first step of normal beta ox)

47
Q

Beta OX: how many less ATP will linoleic acid produce? 18: 2 delta 9,12)

A

5
one round of cis 3 (beta-gamma) bond correction
one round of delta4 bond correction

48
Q

Beta OX: what is the other product in odd chain FA oxidation not seen in even chain FA oxidation?

A

propionyl-CoA

49
Q

Beta OX What is propionyl-CoA converted into by what enzymes (3)?

A

s-methylmalonyl-CoA (via propionyl-CoA carboxylase) then to succinyl-CoA (via methyl malonyl-CoA epimerase or racemase and methyl malonyl-CoA mutase)

50
Q

Beta OX: propionyl-CoA carboxylase cofactor?

A

biotin

51
Q

Beta OX: methyl malonyl-CoA mutase cofactor?

A

B12

52
Q

Where are ketone bodies produced? (organ) When?

A

liver (mitochondria it is the only place with HMG-CoA lysase and only place with high levels of HMG-CoA synthase), fasting and starvation

53
Q

the Ketone body compounds are____ , ____ ,and ____?

A

acetoacetate (primary), beta-hydroxybutyrate, acetone

54
Q

Can the brain use acetyl CoA? Ketone bodies?

A

NO, YES

55
Q

Look at ketone body enzymes on pg 225 of the notes

A

these suck

56
Q

What molecule from beta ox inhibits pyruvate dehydrogenase and activates pyruvate carboxylase?

A

acetyl-CoA

57
Q

What does the TCA cycle stop in ketone body production?

A

The large amount of NADH produced by beta ox inhibits isocitrate dehydrogenase. citrate builds up. in the liver, OAA is converted to malate and leaves the mito for gluconeogen

58
Q

What can cause ketone body production?

A

fasting, heavy alcohol consumption, high fat/low carb diet, and uncontrolled diabetes

59
Q

How is beta-hydroxybutyrate metabolized in extrahepatic tissues? is there an energy cost?

A

Converted back to acetoacetate by beta-hydroxybutyrate dehydrogenase then picks up a CoA from succinyl-CoA becoming acetoacetyl-CoA then thiolase converts it back to acetyl coA. Cost 1 GTP to regenerate succinyl-CoA

60
Q

Why can type 1 DM be considered a disorder of Fatty acid metabolism? What is the result of uncontrolled type 1 DM

A

Because the lack of insulin caused runaway lipolysis, causes metabolic acidosis (diabetic ketoacidosis). Type 2 the amount of blood ketone bodies is not a severe bc some insulin is present so it is called ketosis

U6 MCP (26 decks)

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