High Yield (part III) Flashcards
What is needed in order to digest TGs?
- Bile salts (gallbladder) emulsify fat 2. Pancreatic lipase (needs a co-lipase to function) acts to remove 2 of the FAs (left with 2FAs + monoglycerol) 3. Bile salts form micelles 4. micelles cross the intestinal epithelium 5. FAs activated and recombine with monogycerol to form TGs again 6. TG combines with AboB48 and other lipids to form chylomicrons 7. chylomicrons leave the intestinal cells, enter lymph circulation, then enter blood circulation
what transports DIETARY lipids
chylomicrons = **TG + ApoB48 + cholesterol + lipid monolayer + peripheral apoprotein
How do we transport ENDOGENOUS lipids
A from the liver are turned into TGs and then put into blood for transport by VLDL *insulin stimulates the liver to synthesize VLDL
Name the most common fatty acids ingested as TGs (so there would be 3 in a TG)
palmitate, oleate, stearate (with glycerol as backbone) -note these are ‘long chain FA’ (16 carbons or longer)
Details of Carintine shuttle? pic slide 25
CPT I complex – gets us in a form that can be shuttled across the inner mitochondrial membrane(adds carnitine)
Carnitine acylcarnitine translocase (CAT) actually responsible for the transport
CPT II – removes the carnitine, so we can get oxidation
Alrighty, now the FAs are in the mitochondria matrix, what now? what are we doing?
Beta Oxidation! *The beta oxidation spiral takes FA and generates Acetyl CoA and NADH note: since we are forming NADH it is a good bet that there will be dehydrogenase enzymes in the B-oxidation spiral
The energy yield from β-oxidation of FA is GREAT! what is it?
Number of clevages = n N= #of NADH and FADH2 N+1= # of acetyl CoA **(1.5 ATP/FADH2) **(2.5 ATP/NADH) (10 ATP per acetyl-coA)
Ex: 16-C palmitic acid (do the math bitch)
7 cleavages = 7 FADH2 and 7 NADH 7 x 1.5 ATP/FADH2 + 7 x 2.5 ATP/NADH = 28 ATP Subtract 2 ATP for cleavage of 2 Pi bonds 8 acetyl-coA to use in TCA cycle ~10 ATP per acetyl-coA (80 ATP) So a total of 26 + 80 = 106 ATP per palmitic acid.
One major Regulation of β-oxidation, and 3 others?
-Biggest factor-Demand for energy (fasting, exercise) stimulates B-oxidation (THIS IS THE RATE LIMITING STEP OF B-oxidation, so adding a caratine supplement wont help you burn fat/use more energy unless you exercise/fast) *AMP stimulates (indicating cells energy needs are not met!) -Malonyl CoA inhibits -insulin inhibits (via stimulating Malonyl CoA) -obviously buildup of products inhibit (bc the cells energy need are met, we don’t need B-oxidation (energy) NADH inhibits ATP inhibits Acetyl CoA
What is spontaneous decarboxylation?
Acetoacetate can lose CO2 spontaneously and form acetone in the blood This results in ketoacidosis (acetone smell on the breath is a giveaway!)
Regulation KB synthesis
-like FA synthesis, it’s based on energy needs: *biggest stimulator -energy demand (long fast / exercise) -AMP - stimulates synthesis -high ATP, NADH, insulin (ALL INHIBIT SYNTHESIS OF KB)
WHat the heck is alternate Ketone body metabolism??
Just know that the carbon skeletons of some AA can produce Ketone bodies
- ketogenic amino acids = leucine, lysine
- ketogenic and glucogenic = isoleucine phenylalanine tryptophan tyrosine threonine
What is (are) the major organ(s) acted on by glucagon?
Glucagon works on the live glycogenolysis gluconeogenesis
How does the TCA cycle relate to glycolysis, fatty acid oxidation, ketone body oxidation, and amino acid oxidation?
Each of these metabolic pathways produces Acetyl CoA which enter the TCA cycle for oxidation as oxaloacetate
so all of these result in NADH, FADH2!!! thats what we’re after
A patient has low insulin, what is the effect of low insulin? Do we see evidence of this in our patient’s lab results?
-Insulin stimulates LPL expression and inhibits HSL activity; -Low LPL would lead to high serum VLDL and chylomicrons -Elevated glucagon would also contribute FA to blood (she will have fatty serum)
