Digestion, Transport and Synthesis of Triacylglycerols
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- what is the breakdown of fuel storage by %: muscle glycogen, liver glycogen, protein, and fat
- muscle glycogen (0.4%), liver glycogen (0.2%), protein (14.5%), Fat (85%)
- What is the breakdown of water content in tissues by %: adipose, muscle, glycogen
- adipose (15%), muscle (80%), glycogen(70%)
- Given the water content, where would lose more mass, by losing adipose or muscle?
- Muscle because it's associated with water
- Why do crash diets that are low protein and low carbohydrate work?
- because without amino acid intake we breakdown our own muscle, also loss of mass in the liver due to loss of glycogen with its associated water thus more mass is lost
- On a TAG, where would be more likely to find an unsaturated FA?
- carbon II
- what is the function of a colipase?
- stabilizes the lipase so it does not get denature by the bile salts⬦ thus the lipase can break down TAGs to FA + Glycerol
- What happens to the 2-monoacylglycerol?
- they are used to resynthesize TAGs⬦ and ultimately made into chylomicrons.
- What are chylomicrons?
- they are the vehicle by which insoluble fats can be carried in plasma
- What is an ApoB?
- it is the polypeptide component of the lipoproteins
- Which FA is removed from the TAG by pancreatic lipases
- from C1 and C3
- what is steatorrhea?
- a "floater", excess lipid content in stool⬦ cause could be a) bile duct obstruction⬦ or gall bladder⬦ b) insufficient pancreatic production of lipase⬦ (difference in feces scent would be observed due to bacterial flora growth)
- In FA transport as TAGs, fatty acids must first be activated. How is this accomplished? And what does it become?
- ATP⬦ it becomes fatty acyl CoA
- After the activation of fatty acids to fatty acyl-CoA, how is the TAG made?
- 2 fatty acyl CoA are attached to 2-monoacylglycerol (in a two step process.)
- Why are TAGs broken down, then reassembled?
- So that the end TAG has the longest possible, most hydrophobic FAs on them.
- Why is it that only long chain FAs are attached and not medium chain FFAs?
- Medium chains FFAs don't require lipoproteins for transfer through plasma⬦ instead they are carried by albumin⬦ Long chain FFAs on the other hand must be attached to chylomicrons
- Besides the TAGs and other lipids, what else is attached to chylomicrons?
- Apoproteins
- What are lipoproteins lipases?
- They breakdown the TAGs in chylomicrons so they can be transported into tissues (muscles and adipose)
- Besides chylomicrons, what other type of lipoproteins is there? What is the difference between chylomicrons and _______?
- a) VLDL⬦ b) chylomicrons carry dietary TAGs, thus quantifying the amount of TAG represents the amount of fat in your recent diet.
- Where do the TAG held in VLDL come from?
- the liver
- What is the necessary intermediate needed in the liver and adipose tissue in the production of triacylglycerol?
- Glycerol-3-P
- In adipose tissue dihrooxyacetone phosphate (DHAP) is required before glycerol-3-P can be formed, From what precursor is DHAP derived?
- glucose
- Besides converting DHAP, how else can the glycerol-3-P be formed?
- The phosphorylating a glycerol by glycerol kinase
- What is the glycerol-3-P converted into? How is this accomplished? Where can this occur?
- a) a TAG⬦ b) FAs must be added⬦ c) the liver
- What is the name of the TAG intermediate with only two FA (on C1 and C2) and has a phosphate on C3?
- phosphatidic acid, which will go on to make TAG by losing the phosphate and gaining another FA
- Do these glycerol-3-P TAGs become integrated into chylomicrons or VLDL?
- VLDL⬦ they are synthesized TAGs not dietary
- Since the liver prefers to use fatty acids as an energy source, what does it use glycolysis for?
- to generate carbons (glycerol-3-P) for compounds like TAGs
- what are the healthy fates of VLDLs?
- They give rise to IDLs and LDL and intermediate density lipoproteins (IDL)
- What is the down side of the fate of VLDLs?
- They give rise to oxidized products which can be taken up by cells lining blood vessels, which can lead to atherosclerosis (clogging or narrowing of arteries by cholesterol)
- Increased alcohol consumption gives rise to excess cellular NADH, the high NADH:NAD+ ratio causes the reduction of DHA P to Glycerol-3-P. How is this responsible for hepatic steatosis (fatty liver)?
- Glycerol-3-P is a precursor in TAG synthesis.
- How does the increased insulin:glucagon ratio cause the deposition of fat in adipose tissue?
- insulin UP --> GLUT-4 on adipose UP --> favoring DHAP to Glycerol-3-P⬦ more TAGs
- Which hormone increases secretion of LPL from adipocytes?
- insulin, this makes sense since insulin positively regulates storage of fats
- Besides insulin, what else increases the activity of LPL?
- apoproteins, chylomicrons, and VLDL
- What is hormone sensitive lipase (HSL)? When is it activated? and which insulin:glucagon ratio activates it?
- a) breaks down TAG to FAs and glycerol in adipose during the fasted state⬦ b) It is activated when it is phosphorylated⬦ c) Since a high insulin:glucagon ratio corresponds to the activation of protein kinases that is when it's activated.