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SFM (Scientific Foundations of Medicine) > Lecture 5: Lipid Metabolism > Flashcards

Lecture 5: Lipid Metabolism Flashcards

1
Q

What is the major source of carbon for FA synthesis? What are the precursor and end product of FA Synthesis

A

major source: dietary carbohydrates

FA Synth precursor: Acetyl CoA

FA Synth endproduct: palmitic acid

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2
Q

What are the 3 phases of Fatty Acid Synthesis?

A

Phase 1: Cytosolic Entry of ACoA
Phase 2: Generation of Malonyl CoA
Phase 3: FA chain formation

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3
Q

FA Synth Phase I Enzymes

A
  1. Citrate Synthase
    • oxaloacetate and ACoA = citrate
  2. ATP Citrate Lyase
    (+) - glucose, insulin
    (-) - PUFA, leptin
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4
Q

FA Synth Phase II Enzymes

A
  1. Acetyl CoA carboxylase (adds CO2 to ACoA)
    (+) - citrate, insulin
    (-) - glucagon, epinephrine, AMP, palmitate, PUFA
  • RATE LIMITING ENZYME (needs BIOTIN)
  • 2C converted to 3C
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5
Q

What does malonyl CoA regulate?

A
  • inhibits carnitine acyltransferase (FA degradation RLS)

- prevents synthesis and degradation from occurring simultaneously

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6
Q

FA Synth Phase III Enzyme

A
  1. Fatty Acid Synthase
    (+) - insuling, glucocorticoid hormones
    (-) - PUFA

multi-enzyme complex, 2 identical dimers, head to tail

  • Acyl Carrier Protein (ACP) moves things between each of the 7 enzymes on one half of the dimer
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7
Q

Fatty Acid Synthesis Reactions

A
  1. Condensation (acetyl and malonyl groups)
  2. Reduction (ketoacyl –> hydroxyl)
  3. Dehydration (hydroxyl –> trans-enone)
  4. Reduction (4 chain fatty acyl group)

repeats 6 more times

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8
Q

Regulation of Fatty Acid Synthase (allosteric and induction/repression at gene level)

A

Allosteric:
(+) - phosphorylated sugars

Gene Level:
(+) - insulin, glucocorticoid hormones, hi carb/low fat
(-) - high fat diets, PUFA

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9
Q

Synthesis of Longer Chain FA and carbon donors

A
  • elongation in SMOOTH ENDOPLASMIC RETICULUM
  • lengthened 2 carbons at time (NADPH reducing power)

SER –> Malonyl CoA (carbon donor)
Mitochondria –> Acetyl CoA (carbon donor)

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10
Q

FA Desaturation

A
  • Acyl CoA Desaturases (4 desaturases - 4,5,6,9)

cannot introduce DB past carbon 9 and 10
- require omega 3 and 6 fatty acids (Essential FA)

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11
Q

Essential Fatty Acids (2) and what they can make

A

Omega 6: Linoleic Acid (18:2)

  • can make arachidonic acid (20:4)
  • precursors for EICOSANOIDS

Omega 3: Linolenic Acid (18:3)
- can make EPA (20:5) and DHA (22:6)

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12
Q

TAGs and Energy Storage

A
  • TAGS contain 6.75 times as much energy as glycogen (carbs)

normal man: 40 Cal glucose, 600 Cal glycogen, 24,000 Cal protien, 100,000 Cal TAGs

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13
Q

3 main sources of TAGs

A
  1. Dietary TAGs (intestinal processing)

2. De Novo TAGs (hepatocytes and adipocytes)

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14
Q

Intestinal TAG Synthesis

A
  • dietary TAGS –> MAG and FFA in intestinal lumen
  • MAG used as backbone (2 fatty acyl CoA added) in order to make TAG
  • TAGs packaged w/apolipoproteins and other lipids to make Chylomicrons (released to lymphatic system and enter blood)
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15
Q

Hepatocyte TAG Synthesis and enzymes

A

enzymes: fatty acid acyl synthetase, G3P dehydrogenase, glycerol kinase

  • glucose/glycerol form G3P (used as TAG backbone)
  • FFA (liver) added to G3P to form TAGs
  • packaged w/apolipoproteins/lipids to make VLDL (released into bloodstream)
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16
Q

Adipocyte TAG synthesis and enzymes

A

enzymes: G3P dehydrogenase, capillary lipoprotein lipase (+: insulin)

  • glucose to G3P (backbone)
  • FFA (chylomicrons/VLDL) added to G3P to make TAGs
17
Q

4 major lipases in TAG breakdown

A
  1. adipose triglyceride lipase (ATGL)
    • TAG –> DAG
  2. hormone sensitive lipase (HSL)
    • DAG –> MAG
  3. lipoproteinlipase (LPL)
    • DAG –> MAG
  4. monoacylglycerol lipase (MAG Lipase)
    • MAG –> DAG
18
Q

Molecules that regulate HSL

A
  1. Hunger and Exercise (phosphorylate HSL - PKA)
    • Hunger (+) –> glucagon
    • Exercise (+) –> epinephrine
  2. Fed Status (dephosphorylate HSL - protein phosph 1)
    • High carb meal (-) –> insulin
19
Q

What is a perilipin and what does it do?

A
  • family of proteins, coat lipid droplets in adipocytes/muscle cells
  • REGULATE LIPOLYSIS (control physical access to HSL)
  • Overexpression: inhibit lipolysis and knock-out has converse effect
  • obesity treatment target
20
Q

Fatty Acid Activation Phase I (Mitochondrial Transport) and enzymes

A
  • LCFA/VLCFA need to be actively transported into mito
    enzymes: fatty acyl CoA synthetase, Carnitine palmitoyltransferase I (CPT1 –> RLS), Carnitine-acylcarnitine translocase (CACT), Carnitine palmitoyltransferase II (CPT II)
21
Q

Mitochondrial Membrane permeability to Fatty Acids

A

Outer Mito Membrane - not permeable to FA
- FA to FA CoA

Inner Mito Membrane - not permeable to FA CoA

  • FA CoA to FA carnitine
  • CPT1 adds carnitine (rate limiting enzyme)
  • CPT2 removes carnitine
  • CACT moves carnitine across inner mito membrane
22
Q

What is the rate limiting enzyme of Fatty Acid Oxidation?

A

carnitine palmitoyltransferase I

(-) - malonyl CoA

23
Q

What are the 4 steps of B oxidation of Fatty Acids and what do they generate?

A

steps: oxidation, hydration, oxidation, thiolysis

1st oxidation enzyme: Acyl CoA Dehydrogenase (ACAD)

  • four types: short, medium, long, very long
  • MCAD is the most common defective

generates: Acetyl-CoA (8), NADH (7), FADH2 (7)

24
Q

How much energy does NADH, FADH2, and Acetyl CoA produce?

A

NADH –> 2.5 ATP per mol

FADH2 –> 1.5 ATP per mol

Acetyl CoA –> 10 ATP per mol

25
Q

Beta Oxidation of odd numbered FAs

A
  • metabolized until Propionyl CoA (3C)
  1. Propionyl CoA Carboxylase
    • ATP, generates Methylmalony CoA
  2. Methylmalonyl CoA Mutase
    • generates Succinyl CoA

Succinyl CoA enters TCA cycle

26
Q

Beta Oxidation of Unsaturated FAs

A
  • metabolized until unsaturation reached

- Reductase removes DB, Isomerase moves disruptive bond

27
Q

MCAD Deficiency

A
  • impairs breakdown of medium chain fatty acids (MCFA)
  • leads to secondary carnitine deficiency (excessive MCA carnitines in urine)
  • C8 FA accumulates in liver, poisonous, disrupts urea cycle, inc. ammonia lvls

patient depends on GLUCOSE as energy source

treatment (preventative) –> avoid fasting, situations that rely on FA Beta Oxidation

28
Q

What are ketone bodies and what are examples?

A
  • water soluble, acidic (produced in Liver)

ex: Acetoacetate –> B-Hydroxybutyrate and Acetone

29
Q

Fuel Supply during fasting and starvation

A
  1. first few hours: blood glucose, then glycogen, then gluconeogenesis (liver)
  2. 1 day fasting: TAGs (adipose); FFA –> B oxidation
  3. 3 days fasting: ketone bodies and muscle proteins broken down
  4. 1-2 weeks starvation: brain use ketone bodies
  5. 2-3 weeks starvation: TAGs depleted, proteins main source
30
Q

Ketoacidosis during Starvation and Diabetes

A
  • pathological occurs: glucagon/insulin ratio increased, favoring FA breakdown
  • inc. gluconeogenesis (reduced oxaloacetate
  • inc. ketone bodies
  • occurs during fasting, pregnancy, in babies, prolonged exercise, ketogenic diet

ketone bodies lower blood pH (acidosis), inc. excretion
acetone exhaled from breath (fruity)

SFM (Scientific Foundations of Medicine) (20 decks)

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