Lipids, Fats, Metabolism Flashcards
(30 cards)
Features of lipids in bio membrances
amphipathic
fluidity effected by composition of membrane
What changes fluidity?
more unsaturated –> more fluid
more cholesterol –> less fluid
inc. FA chain length –> less fluid
TG Composition and Amphipathy
Polar Head group = phosphate + alcohol moeity attached to C3
nonpolar FA tail = C1 usually saturated FA, C2 usually unsaturated FA
Why are fats the most efficient energy storage molecule?
- more reduced
- stored in a near anhydrous form
Draw the general stx of a TG
Whats the first regulated step in lipolysis?
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
When is Lipolysis stimulated?
Fasting (Low I/G)
Prolonged exercise (adrenaline)
The FA product of Lipolysis does what?
transported to blood … associates with plasma albumin … transported to tissues for oxidation
What happens to the glycerol product of lipolysis?
It can’t be converted to glycerol-3-P in adipose b/c adipose has no glycerol kinase…
transported to liver for gluconeogenesis
What effect does insulin have lipolysis?
Insulin is antiolipolytic…
it activates cAMP phosphodiesterase.
It is better at inhibiting lipolysis in peripheral fat than visceral fat.
What tissues do beta-ox?
muscle, liver, kidney
first step in cytoplasm, beta-ox in mito matrix
What is the rxn of fatty acid activation?
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
How does FACoA enter mito matrix?
Draw out beta-ox.
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
How is beta-ox under respiratory control?
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.
Calculate ATP production from a 16 C FA
- 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
What happens if the FA has an odd number of C?
Oxidized normally until C5 chunk formed
Thiolytic cleavage gives acetylCoA + propionyl CoA
propCoA converted to succinylCoA, enters metabolism
What are the ketone bodies?
Acetoacetate
beta-hydroxybutyrate
acetone
Under what conditions are ketone bodies synthesized?
When lipolysis is activated and FA are being utilized as fuel…
prolonged exercise or fasting
Where and why is ketone body synthesis
liver mitochondria bc of a build up of acetylCoA
Why doesn’t acetyl coA product of FA utilization just go through TCA?
TCA is slowed at citrate synthase rxn due to three allosteric inhibitors: citrate, NADH, FACoA
How are two Acetyl CoA converted to acetoacetate, acetone, and beta-hydroxybutyrate?
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)
What happens to acetoacetate and beta-hydroxybutryate?
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
Describe ketosis and consequences
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)
