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Biochem Exam 3 > FA, Ketone Body and TAG Metabolism > Flashcards

FA, Ketone Body and TAG Metabolism Flashcards

1
Q

How do FAs exist?

A

1) Free

2) FA esters (covalently linked to something)

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2
Q

What are some FA functions?

A
  • Free FAs in fasting state transported in plasma on albumin
  • In liver and muscle oxidized -> energy and ketone body synthesis
  • Structural component of membrane lipids (glycolipids and phospholipids)
  • Precursor of hormone-like prostaglandins
  • Stored in white adipose tissue as major energy reserve
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3
Q

What is the structure of a FA?

A

Hydrophobic hydrocarbon chain + terminal hydrophilic carboxyl group
-Ampipathic but predominantly hydrophobic

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4
Q

What makes up 90% of plasma FAs?

A

FA esters (TAG, cholesteryl esters, and phospholipids) in lipoprotein particles

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5
Q

What is a saturated FA?

A

No double bonds

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6
Q

What is a mono-/polyunsaturated FA?

A

1 or more double bond

-All cis in nature

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7
Q

What is the number 1 trans fat in USA?

A

McDonald’s fries

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8
Q

What does a double bond do?

A
  • Decrease melting temp.
  • Increase chain length
  • Increase Tm
  • Helps maintain fluid nature of membranes
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9
Q

What number of Cs predominates?

A

Even numbers (16, 18, 20); >22 found in brain

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10
Q

What is palmitic acid and how many double bonds does it have?

A

Product from us making fat

-16:0 (16 Cs; no double bonds - saturated)

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11
Q

What is arachidonic acid?

A

Seen in drugs to prevent pain

  • 20:4
  • Omega-6 FA (terminal double bond is 6 bonds in from omega-end or the carbon of terminal methyl group)
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12
Q

How many double bonds does acetic acid have?

A

None

-2:0

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13
Q

What are the essential FAs?

A

1) Linoleic acid (18:2) - arachidonic precursor -> substrate for prostaglandin
2) alpha-Linoleic acid (18:3) - precursor of omega-3 FAs (growth and development)

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14
Q

What is de novo synthesis?

A

Carbs and proteins from diet in excess -> converted to FAs -> stored as TAGs

  • In liver cytosol
  • Incorporates Cs from acetyl CoA into growing FA chain, using ATP and NADPH
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15
Q

After eating pasta/bread, the excess glucose is sent to liver and increased insulin and glucose stimulates what?

A

Glycolysis -> pyruvate

  • Pyruvate is taken into mitochondria
  • Pyruvate -> OAA by pyruvate carboxylase
  • Pyruvate -> Acetyl CoA by PDH
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16
Q

What does the enzyme citrate synthase do?

A

Acetyl CoA + OAA -> Citrate

-Acetyl CoA cannot come out of mitochondria alone, but citrate can

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17
Q

What does enzyme ATP citrate lyase do?

A

Splits citrate into OAA + cytosolic acetyl CoA

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18
Q

What does enzyme acetyl CoA carboxylase do?

A

Carboxylation of acetyl CoA -> Malonyl CoA

  • 2 C -> 3 C
  • Main regulated/rate-limiting step
  • Uses bicarbonate and ATP
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19
Q

What is acetyl CoA carboxylase activated by?

A

Citrate

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20
Q

What is acetyl CoA carboxylase inhibited by?

A

Palmitoyl CoA

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21
Q

What does enzyme FA Synthase do?

A

Malonyl CoA -> Palmitate

-Uses NADPH and takes 2 Cs at a time until you have 16 -> Palmitate

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22
Q

How is palmitate made into TAG?

A

Palmitate -> Palmitoyl-CoA

-Used w/ glycerol 3-phosphate (from glycolysis) to make TAG

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23
Q

What is a lipoprotein (VLDL) made from?

A

Fat we created from excess carbs; made in liver!!

-In contrast to chylomicrons made in intestinal epithelial cells from dietary fat

24
Q

Metformin is used in the treatment of type-2 diabetes. How does it work?

A

Lowers serum [TAG] through inhibition of acetyl CoA carboxylase (by phosphorylation) and fatty acid synthase expression
-Also lowers blood glucose by increasing AMPK-mediated uptake of glucose by muscle

25
Q

In a well fed state and in the cytosol, what is required to make fatty acids?

A

NADPH

26
Q

How can NADPH be made?

A

1) Pentose phosphate pathway

2) Cytosolic conversion of malate -> pyruvate by cytosolic malic enzyme (uses NADP+ to make NADPH)

27
Q

What is NADPH used for?

A
  • Synthesis of FAs, steroids and cholesterol
  • Cytochrome p450 sx
  • Detoxification of ROS intermediates
28
Q

How are FAs stored as components of TAG?

A

FAs esterified through carboxyl groups -> lose neg. charge -> “neutral fat”
-Coalesce w/ adipocytes, form large oily droplets -> major body energy reserve

29
Q

Acylglycerol solids at room temp are ____ ; liquids at room temp are ____.

A

Fat; oil

30
Q

What is required to make TAG?

A

Glycerol 3-phosphate

31
Q

How is G3-P made in the liver and adipose tissue?

A

From glucose, using glycolytic pathway to produce DHAP -> reduced by Glycerol 3-P Dehydrogenase -> G3-P

32
Q

How is G3-P made ONLY in the liver?

A

Glycerol kinase

-Can take free glycerol and add a phosphate + either DHAP or glycerol kinase -> G3-P

33
Q

What must happen to FAs in order to be made into TAG?

A

Must be activated by Fatty Acyl CoA Synthesases -> bound to CoA

34
Q

What is TAG made from?

A

Glycerol 3-P + 3 Fatty Acyl CoAs

35
Q

How are most of TAG from liver exported?

A

In VLDLs

36
Q

In the fasting state what causes release of FAs from fat?

A

Hormone-sensitive lipase activated by PKA via Adenylyl cyclase

37
Q

What binds to receptor ultimately activating hormone-sensitive lipase?

A

[Epinephrine/Glucagon] high -> Glucagon binds -> ATP w/ adenylyl cyclase -> cAMP + PPi -> signal transduction -> activate protein kinase A -> turns on hormone-sensitive lipase (made active by phosphorylation)

38
Q

What does HSL break TAG down into?

A

Glycerol + 3 FAs

39
Q

What is the fate of glycerol?

A

Transported to liver, phosphorylated and used to form TAG or converted to DHAP -> glycolysis/gluconeogenesis -> glucose

40
Q

What is the fate of free (unesterified) FAs?

A

Sent one by one bound to albumin -> tissues -> activated to CoA derivatives, oxidized for energy in mitochondria
-Brain does not use FAs for energy (prefers glucose)

41
Q

How do we get energy from FAs?

A

Beta-oxidation of FAs

  • 1 FA = 129 ATP!
  • Inside the mitochondria
42
Q

What is removed in beta-oxidation of FAs?

A

2-C fragments successively removed from carboxylate end of fatty acyl CoA

  • If 16 C -> happens 7x
  • Product: NADH and FADH2 (made first, can be send to ETC to make ATP), and Acetyl CoA (sent to TCA to make ATP)
43
Q

Why is carnitine required in the beta-oxidation of FAs?

A

LC Fatty acyl-CoA cannot cross to go inside mitochondria

  • Carnitine is synthesized in mitochondria -> CPT1 will temporarily transfer LC fatty acyl-CoA to Carnitine to transport it inside mitochondria
  • Only way you can get energy from fat
44
Q

How is carnitine removed once inside mitochondria?

A

Carnitine Palmitoyl-Transferase II (CPTII)

-Free LC fatty acyl-CoA -> can now burn fat for energy

45
Q

What inhibits CPT1?

A

Malonyl CoA

-Because this is when you are making fat, you don’t want to burn fat

46
Q

What happens in the beta-oxidation of FAs w/ odd number of Cs?

A

Same steps until final 3 Cs reached:

  • Propionyl CoA -> Succinyl CoA (by Propionyl CoA Carboxylase)
  • Only way sugar can be made from FAs
  • Requires Vitamin B12 and Biotin
47
Q

What does liver mitochondria convert acetyl CoA to?

A 
Ketone bodies (KBs)
-Transported to tissues and reconverted to acetyl CoA
48
Q

What is the importance of KBs?

A

1) Soluble and easy to get out
2) Produced when acetyl CoA in liver is in excess
3) Used in proportion to blood concentration (muscle, intestine, kidney)
4) Spare glucose during starvation

49
Q

What happens when the liver is flooded w/ FAs in fasting state?

A

Acetyl CoA inhibits Pyruvate Dehydrogenase and activates Pyruvate Carboxylase

  • OAA used for gluconeogenesis
  • Acetyl CoA channeled to KB synthesis
  • Liver will make KBs but cannot use them
50
Q

What are the products of beta-oxidation of FAs to Acetyl CoA in the liver?

A

Acetoacetate + Beta-Hydroxybutyrate (Ketone bodies)

-2 C -> 4 C

51
Q

What happens to KBs in the muscle?

A

Broken down into Acetoacetate + Beta-Hydroxybutyrate -> Acetyl CoA (used for TCA -> ATP)
-4 C -> 2 C

52
Q

What disease is correlated with excessive production of KBs?

A

Uncontrolled type 1 Diabetes Mellitus

53
Q

What does increased [glucagon] in Diabetes Mellitus cause?

A

Signals breakdown of FAs from fat cells and increase lipolysis to increase FAs in blood -> increased beta-oxidation in liver, increased KBs made in liver -> ketoacidosis

54
Q

What causes the fruity odor on breath in uncontrolled type 1 DM?

A

KBs can spontaneously decarboxylate -> increased acetone production

55
Q

What is ketonemia?

A

Increased [KBs] in blood

56
Q

What is ketonuria?

A

Increased [KBs] in urine

-Eventually follows ketonemia

Biochem Exam 3 (7 decks)

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