[FMS] NAM - fat as fuel Flashcards
what are the 3 biological function of lipids
- Components of cell membranes - (phospholipids & cholesterol)
- Precursors of hormones
cholesterol → steroid hormones
arachidonic acid → prostaglandins
3. Long term fuels (triglycerides)
how are triglycerides stored
triglycerides stored as large fat droplets in the fat cells of adipose tissue
what are the common fatty acids and their ratios
remember ‘pimsols’ = PSOLL
- How is stored triglyceride fat in the adipose tissue broken down?
remember: TAG, DAG, MAG ‘The Disgusting Man’
How is glycerol metabolised in most tissues
Enters glycolysis pathway for conversion to pyruvate, then
into TCA cycle foroxidation to CO2
How is glycerol metabolised in liver/ starvation
Enters glycolysis pathway and is converted to glucose by gluconeogenesis
where does the b oxidation of fatty acids occur
mitochondrial matrix
How are long chain fatty acids activated?
activated in the cytosol by the addition of Fatty acyl-CoA synthetase.
Outline how fatty acyl-CoA is transported into the mitochondria?
CARNITINE SHUTTLE
why is it called the b-oxidation pathway?
Called β-oxidation because the β-carbon undergoes oxidation to produce a carbonyl group (carbon double-bonded to oxygen).
where is CPTI?
outer mitochondrial membrane
where is CACT?
inner mitochondrial membrane
where is CPTII?
mitochondrial matrix
what does one round of b-oxidation produce
One round of β-oxidation produces acetyl-CoA and a fatty acyl-CoA that is 2 carbons shorter
- the 2 carbons are now carried by acetyl-CoA.
what are the steps of b-oxidation including the enzymes and products lost
how many repeats does a C16FA pass through and how many NADH and FAHD2, snd acetyl coA is produced in b-oxidation?
Fatty acid with 16 C atoms
will pass through 7 repeats
of b-oxidation pathway
producing 7 NADH, 7 FADH2, and 8 acetyl coA
REMEMBER: beta oxidation of fatty acids makes:
1 acetyl CoA
1 NADH
1 FADH2
what is the total ATP yield from fatty acid oxidation, why is 2 subtracted from the total amount?
106/107
its originally 108 but -2 because 2 ATP is used in activation stage
3 ways fat metabolism can be regulated
- Release of fatty acids from adipose tissue
(adrenaline & glucagon activate lipase enzyme) - Rate of entry into mitochondria via carnitine shuttle
- Rate of reoxidation of cofactors NADH & FADH2 by Electron Transport Chain
How are odd-numbered fatty acids metabolised?
- If we break down an odd numbered fatty acids we end up with 3 carbons.
- To break this down you have to use ATP so it is not as energetically favourable as breaking down an even-numbered carbon.
– You then have to do 2 conversion reactions and you need to add carbon. - This forms succinyl-coA which enters the TCA cycle.
when does ketogenesis occur in fat metabolism
in starvation
in Type I diabetes
^ ie when fat metabolism is the main source of energy
outline how ketone bodies are formed
increased fatty avid oxidation = increased acetyl CoA
increased acetyl CoA exceed the TCA cycle capacity, Excess Acetyl CoA is converted into ‘ketone bodies’ and released as acetoacetate and β hydroxybutyrate into the bloodstream
They can be taken up by cells for utilisation.
what are 2 ketone bodies
acetoacetate
β hydroxybutyrate
most cell types can use ketone bodies, what intermediates do they get converted into for TCA cycle?
acetyl CoA and succinate
- what is the fuel for human brain? why?
glucose
Brain cannot utilise fatty acids because they can’t get across the blood brain barrier – instead it uses glucose and small amount of ketone bodies (‘emergency fuel’)
- what are the major muscle fuels?
glc, FA (ketone bodies)
- what do muscles and brain lack?
glucose-6-phosphatase
- what does the liver do?
provides brain, muscle and other organ fuel
Red blood cells cannot utilise fatty acids or ketone bodies, use glucose only, why?
they don’t have mitochondria so they can’t do any of the processes.
How are free fatty acids transported in the blood? They are:
- carried by albumin.
- carried by carnitine.
- carried by chylomicrons.
- carried by low- and high-density lipoproteins (LDLs and HDLs)
- freely soluble and do not require a carrier.
1
What are the three main biological function of lipids?
- Components of ribosomes, precursor for steroid hormones, and long-term fuel storage.
- Components of membranes, precursor for steroid hormones, and short-term fuel storage.
- Components of membranes, precursor for steroid hormones, and long-term fuel storage.
- Components of the nucleic acids, precursor for peptide hormones, and long-term fuel storage.
- Components of membranes, precursor for peptide hormones, and long-term fuel storage.
3
Fatty acids with an odd number of carbons undergo β-oxidation until three carbons of the fatty acid remain. This three-carbon unit (propionyl-CoA) is then converted to:
- succinyl-CoA.
- acetyl-CoA.
- enoyl-CoA.
- pyruvate.
- glycerol.
1
A reaction sequence that takes place in mitochondria when fatty acids are broken down for energy can be described as:
- an oxidation followed by a hydration followed by a reduction.
- an oxidation followed by an oxidation followed by a decarboxylation.
- an oxidation followed by an oxidation followed by a hydrolysis.
- an oxidation followed by a reduction followed by a hydrolysis.
- an oxidation followed by a hydration followed by an oxidation.
5
A deficiency that prevents someone from synthesising carnitine could cause:
- Accumulation of lipid droplets in the mitochondrial matrix of liver cells
- Accumulation of lipid droplets in the cytosol of liver cells
- A decrease in free long chain fatty acids circulating in the blood.
- Increased beta -oxidation and reduced storage of long chain fatty acids in liver cells
- Increased conversion of long chain fatty acids to glucose in the liver.
ANSWER = 2
EXPLANATION:
1. Accumulation of lipid droplets in the mitochondrial matrix of liver cells: This is unlikely because the deficiency would hinder the transport of fatty acids into the mitochondria for beta-oxidation, leading to reduced fatty acid metabolism within the mitochondria, not accumulation of lipid droplets there.
- Accumulation of lipid droplets in the cytosol of liver cells: This is a plausible outcome because if fatty acids cannot be transported into the mitochondria for beta-oxidation, they may accumulate in the cytosol of liver cells, leading to the formation of lipid droplets.
- A decrease in free long-chain fatty acids circulating in the blood: This is plausible because if fatty acids are not being transported into the mitochondria for beta-oxidation, they may remain in other forms (e.g., esterified) and not circulate as free long-chain fatty acids.
- Increased beta-oxidation and reduced storage of long-chain fatty acids in liver cells: This is unlikely because a deficiency in carnitine synthesis would hinder beta-oxidation, not increase it.
- Increased conversion of long-chain fatty acids to glucose in the liver: This is unlikely because a deficiency in carnitine synthesis would disrupt beta-oxidation, which primarily generates energy from fatty acids rather than converting them to glucose.
So, the most likely outcomes of a deficiency in synthesizing carnitine are options 2 (accumulation of lipid droplets in the cytosol of liver cells) and 3 (a decrease in free long-chain fatty acids circulating in the blood).
how are intermediates in b oxidation presented
CoA thioesters
how is the biological energy of fatty acids conserved in b oxidation
conserved via:
- transfer of 2H atoms to the cofactors NAD+ and FAD to make NADH and FADH2
how many enzyme reactions are involved in b oxidation and whats removed during the process?
4 enzyme reactions result in the removal of 2 carbon unit as acetyl CoA
what are the stages of beta oxidation
activation
oxidation
hydration
oxidation
thiolysis
what can inhibit carnitine acyltransferase
malonyl CoA
which metabolic intermediate inhibits the transport system but allows newly synthesised fatty acid to enter mitochondria for oxidation
Malonyl CoA
