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Biochem Block 2 > Lipids, Fats, Metabolism > Flashcards

Lipids, Fats, Metabolism Flashcards

1
Q

Features of lipids in bio membrances

A

amphipathic

fluidity effected by composition of membrane

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2
Q

What changes fluidity?

A

more unsaturated –> more fluid

more cholesterol –> less fluid

inc. FA chain length –> less fluid

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3
Q

TG Composition and Amphipathy

A

Polar Head group = phosphate + alcohol moeity attached to C3

nonpolar FA tail = C1 usually saturated FA, C2 usually unsaturated FA

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4
Q

Why are fats the most efficient energy storage molecule?

A
  1. more reduced
  2. stored in a near anhydrous form
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5
Q

Draw the general stx of a TG

A
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6
Q

Whats the first regulated step in lipolysis?

A

Glucagon/Adrenalin inc. cAMP…

PKA activated …

Hormone sensitive triglyceride lipase and Hormone sensitive diglyceride lipase activated by PKA …

non-hormone sensitive lipases break down MG + FA

TG (H2O)–> DG + FA (H2O)–> MG + FA (H2O)–> Glycerol + FA

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7
Q

When is Lipolysis stimulated?

A

Fasting (Low I/G)

Prolonged exercise (adrenaline)

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8
Q

The FA product of Lipolysis does what?

A

transported to blood … associates with plasma albumin … transported to tissues for oxidation

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9
Q

What happens to the glycerol product of lipolysis?

A

It can’t be converted to glycerol-3-P in adipose b/c adipose has no glycerol kinase…

transported to liver for gluconeogenesis

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10
Q

What effect does insulin have lipolysis?

A

Insulin is antiolipolytic…

it activates cAMP phosphodiesterase.

It is better at inhibiting lipolysis in peripheral fat than visceral fat.

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11
Q

What tissues do beta-ox?

A

muscle, liver, kidney

first step in cytoplasm, beta-ox in mito matrix

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12
Q

What is the rxn of fatty acid activation?

A

RCOOH (ATP)–>(PPI) RCOO-AMP-enz (CoASH)–>(AMP) RCO-SCoA

E = fatty acylCoA synthase

PPi (H2O)–> 2Pi drives rxn forward

Requires two ATP total bc AMP product needs to be converted back to ATP….

AMP + ATP –> 2ADP –> 2 ox. phosphorylations

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13
Q

How does FACoA enter mito matrix?

A
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14
Q

Draw out beta-ox.

A

alkane (FAD)–>(FADH2) alkene (H2O)–> alcohol (NAD)–>(NADH2) ketone (HS-CoA) –> AcetylCoA + shortened chain

Overall: if you have a 16 C FA, you will get 8 Acetyl-CoA, 7 NADH, 7 FADH2

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15
Q

How is beta-ox under respiratory control?

A

physical link between beta-ox and e- transport:

FADH2 is never released from acyl-coA dehydrogenase (bound to inner mito membrane), 2 e- are tranferred directly to CoQ. With no ADP, there will be no e- transport, and no FAD.

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16
Q

Calculate ATP production from a 16 C FA

A
  • 7 repetitions of beta-ox: 8 acetyl CoA, 7 NADH, 7 FADH2*
  • 8 ox. of acetylCoA by TCA: 16 CO2, 24 NADH, 8 FADH2*

8 non-oxphos’s of GDP in TCA = 8 ATP

31 NADH through oxphos = 93 ATP

15 FADH2 through oxphos = 30 ATP

FA activation = -2 ATP

TOTAL= 129 ATP

17
Q

What happens if the FA has an odd number of C?

A

Oxidized normally until C5 chunk formed

Thiolytic cleavage gives acetylCoA + propionyl CoA

propCoA converted to succinylCoA, enters metabolism

18
Q

What are the ketone bodies?

A

Acetoacetate

beta-hydroxybutyrate

acetone

19
Q

Under what conditions are ketone bodies synthesized?

A

When lipolysis is activated and FA are being utilized as fuel…

prolonged exercise or fasting

20
Q

Where and why is ketone body synthesis

A

liver mitochondria bc of a build up of acetylCoA

21
Q

Why doesn’t acetyl coA product of FA utilization just go through TCA?

A

TCA is slowed at citrate synthase rxn due to three allosteric inhibitors: citrate, NADH, FACoA

22
Q

How are two Acetyl CoA converted to acetoacetate, acetone, and beta-hydroxybutyrate?

A

2 acetylCoA condense, realeasing HSCoA..

the product is hydrolyzed and another acetylCoA is added to it giving HMGCoA…

an acetylCoA is removed giving acetoacetate and acetone…

acetoacetate is reduced to beta-hydroxybutryate (w/ NADH+H)

23
Q

What happens to acetoacetate and beta-hydroxybutryate?

A

transported to extrahepatic (mostly skeletal muscle and heart)

In mito:

beta-hydroxybutryate oxidized to acetoacetate by beta-hydroxybutyrate dehydrogenase …

acetoacetate reats w/ succinylCoA to give acetoacetylCoA and succinate…

acetoacetylCoA cleaved to acetylCoA which enters TCA

24
Q

Describe ketosis and consequences

A

Excess build-up of ketone bodies in blood (ketosis) which then spills over into the urine (ketonuria)….

results in the accumulation of H+ (acidosis)…

ketoacidosis can be severe enough to cause unconsciousness (diabetic coma, starvation)

25
Q

Can ketone bodies be used for gluconeogenesis?

A

No bc acetylCoA carbons derived from KB are oxidized to two CO2 in TCA.

26
Q

Give all the steps from low I/G to ketone body synthesis

A
  1. inc. cAMP, activation of PKA, activation of hormone sensitive lipase, FA/glycerol released to blood (adipose)
  2. FA taken up by liver, muscle, others and activated. Transported to mito via CoA:carnitine acyl transferase bc low malonylCoA
  3. FA keeps ATP/ADP, NADH/NAD high. FA ox. limited only by NAD and ADP pools
  4. AcetylCoA accumulates in liver mitos bc citrate synthase inhibited by NADH, citrate, FACoA
  5. Inc. acetylCoA leads to KB synthesis in liver mitos. KB used by fuel.
27
Q

What is the name of the fatty acid utilization transcriptional regulator sites and factors?

A

peroxisome proliferator response element (PPRE)

peroxisome proliferator activator receptor (PPAR)

28
Q

What genes do PPAR/PPRE upregulate/downregulate?

A

lipoprotein lipase

fatty acid transport proteins

CoA:carnitine acyl transferase

fatty acylCoA dehydrogenase

ETS/TCA enzymes

29
Q

What are the important sites of PPAR regulation?

A

Liver, skeletal muscle, heart, adipose

30
Q

How do PPAR act?

A

PPARs bind FA and related compounds as ligands and regulate synthesis of fatty acid utilization proteins.

Biochem Block 2 (1 decks)

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