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30 Cards in this Set
- Front
- Back
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Fat is stored in adipocytes as triacylglycerol. What is it broken down by? |
Adipose triacylglycerol lipase, diacyglycerol lipase, and monoacylglycerol lipase |
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What is the product of the partial oxidation of the fatty acyl oleic acid, 18:1(Δ9) has undergone 3 cycles of β-oxidation? |
Each cycle of β-oxidation releases 2 carbons from the fatty acyl chain, resulting in a 12C fatty acyl chain with the cis double bond now between C3 and C4 |
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How is a cis-Δ3-enoyl-CoA treated in β-oxidation? |
The cis-Δ3-enoyl-CoA is converted into a trans-Δ2-enoyl-CoA by enoyl-CoA isomerase, so that the monounsaturated fat can undergo the remaining steps of oxidation (specifically so that the now trans2-3 double bond can fit into the active site of enoyl-CoA hydratase) |
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What is true about the oxidation of 1 mole of palmitate (16C unsaturated fatty acid; 16:0) by the β-oxidation pathway, beginning with the free fatty acid in the cytoplasm? |
- Activation of the free fatty acid requires the equivalent of two ATPs - Inorganic pyrophosphate (PPi) is produced - 8 mol of acetyl-CoA is formed - Carnitine acts as a mediator of the transport of fatty acids into the mitochondrial matrix |
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What are the direct products of β-oxidation of a fully saturated, straight chain fatty acid of 11 carbons? |
4 molecules of acetyl-CoA, 1 molecule of propionyl-CoA |
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What type of fatty acid would yield the most ATP? |
Fatty acids with the most carbons, and the highest degree of saturation |
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Palmitate is uniformly labelled with tritium (3H). The palmitate is fully oxidized and the carbons are released as CO2. Where does the tritium end up? |
The labelled tritium ends up in H2O |
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The following fatty acid, in which the indicated carbon is labelled with 14C is fed to an animal: 14*CH3(CH2)8COOH Where would the label most likely be recovered in after allowing the fatty acid to undergo β-oxidation? |
A 10 carbon fatty acid is only broken down into acetyl-CoA molecules, so the label ends up in the last molecule of acetyl-CoA formed |
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What is the first enzyme in the β-oxidation of a monounsaturated fatty acid? |
Acyl-CoA dehydrogenase |
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What is the substrates and product(s) for the 2,4-dienoyl-CoA reductase enzyme? |
substrates: A polyunsaturated fat (made by Acyl-CoA dehydrogenase), 2,4-dienoyl-CoA & NADPH product: cis-Δ3-enoyl-CoA |
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Carbon number 10 on the 16 carbon palmitate is the radioactively labelled with 14C. This molecule of palmitate is oxidized under conditions in which the citric acid cycle is operating (and the acetyl-CoA groups from palmitate are being funnelled into the CAC). What will the location of the 14C in the acetyl-CoA? |
The label will be on the methyl carbon of acetyl-CoA. All even numbered carbons of they fatty acid end up as the methyl carbon |
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Which molecules are required and not required for the synthesis of fatty acids? |
required: Acetyl-CoA, Biotin, HCO3-(CO2), Malonyl-CoA not required: NADH |
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If malonyl-CoA is synthesized from CO2 and 14C labelled acetyl-CoA (the label is in both carbons) the, where will the radioactive label be on a 16 carbon fatty acid produced from these two molecules? |
Because the malonyl-CoA is synthesized from the labelled acetyl-CoA and CO2, the incorporation of labelled acetyl-CoA to labelled malonyl-CoA will result in a palmitate molecule thats labelled on every carbon |
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You have a preparation that contains all the enzymes and cofactors necessary for fatty acid biosynthesis once you add acetyl-CoA and malonyl-CoA. If acetyl-CoA that is added is labelled with deuterium, the heavy isotope of hydrogen, and an excess of unlabelled malonyl-CoA are added as substrates, how many deuterium atoms are incorporated into every molecule of palmitate (16:0) and what are their locations? |
Is there is an excess of unlabelled malonyl-CoA, it is not synthesized using the labeled acetyl-CoA. Instead, unlabelled malonyl-CoA is added onto the chain with an initial molecule of labelled acetyl-CoA. The only place the label should exist is on the 16th carbon, as acetyl-CoA only carries hydrogens on its methyl carbons. |
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Which fatty acids can be synthesized by plants but not by humans? |
Fatty acids with unsaturation past C9 (e.g. linoleate [18:2(Δ9,12)]) |
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At the end of 7 cycles of the fatty acid synthase reaction, how long is the fatty acid chain? |
16C |
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At the end of 7 cycles of fatty acid synthesis, which of the carbons most directly come from acetyl-CoA? |
Carbons 15 & 16 |
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What are the biosynthesis precursor in animals of the following unsaturated fatty acids: a) 20:2(Δ11,14) b) 22:1(Δ13) |
a) linoleate 18:2(Δ9,12) b) oleate 18:1(Δ9) |
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What is the methyl group donor in the synthesis of phosphatidylcholine from phosphatidylethanolamine? |
S-adenosylmethionine (Adomet) |
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In the salvage pathway of phosphatidylcholine synthesis, what is the methyl group donor? |
Choline |
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If all the carbons in acetyl-CoA are radio labelled with 14C; what carbons in isopentylpyrophosphate will be labelled? |
All the carbons of isopentylpyrophosphate are labelled; cholesterol synthesis beings with the condensation of 3 acetyl-CoAs, and carbons are not introduced from any other source up to the formation of isopentylpyrophosphate |
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If all the carbons in acetyl-CoA are radio labelled with 14C; what carbons on acetoacetate will be labelled? |
All of them; ketogenesis begins again with the condensation with 3 molecules of acetyl-CoA to HMG-CoA, which is then cleaved by HMG-CoA lyase to form acetoacetate & acetyl-CoA. No carbons other than the labelled carbons from acetyl-CoA are introduced. |
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A new NSAID, SPF is analgesic, anti-inflammatory, and anti-pyretic. The target for SPF is PGH synthase. What is the biological substrate that SPF will be "competing" with for the access of PGHS? |
Arachidonic acid |
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You compare the binding of SPF to its target in the absence and presence of biological substrate arachidonic acid to yield two plots a) On the binding % axis, the binding of which agents is being measured? b) What is being measured on the concentration axis? |
a) The binding of drug candidate SPF to the target enzyme PGHS b) The increased addition of SPF |
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How would a curve that represents the binding in the presence of biological substrate differ from that of one that represents the binding in the absence of a biological substrate? |
In the absence of a biological substrate, SPF does not have to compete for binding to PGHS, so the enzyme-drug interaction is stronger and its Ki is lower. The Ki is higher then the substrate is present to compete with the drug; thus more drug is needed to stimulate the enzyme |
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One of the effects of SPF is drowsiness. What will be the effect on this particular side effect if an individual is taking therapeutic doses of SPF then drinks alcohol? Will there be an increase, decrease, or no change in this side effect? |
There will be an increase in drowsiness. When an individual consumes alcohol, the liver metabolizes alcohol first, leaving other drugs such as SPF unmetabolized longer, increasing the drugs side effects. The intake of alcohol reduces the bodies capacity to metabolize xenobiotics and itself can cause drowsiness. The effects are therefore both elevated and lengthened. |
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You determined the appropriate therapeutic dose of SPF to be 200mg every 4 hours and that at therapeutic doses, cytochrome p450 will hydroxylate and then conjugate SPF with glnucaronic acid. You make a chemical modification that inhibits the hydroxylation of SPF by cytochrome p450 in the liver. What effect, if any will this have n the half life of SPF and why? |
If the hydroxylation of SPF by cytochrome p450 is inhibited, this will prevent the following conjugation (addition of glnucaronic acid) and its oxidation. The drug is not metabolized by cytochrome p450, which extends the half-life of SPF because its concentrations do not decrease by metabolization (1/2 life = amount of time to increase initial drug concentration to 1/2 amount) |
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Another modification is made and SPF seems to be a COX-2 specific inhibitor and will therefore not cause the stomach problems associated with aspirin. Explain why. |
Non-specific inhibitors (aspirin) equally inhibit both COX-1 and COX-2. A dose high enough to inhibit COX-2 to relieve pain will also inhibit COX-1. When COX-1 is inhibited, it no longer can produce gastric mucosa and contribute to homeostasis, resulting in stomach pain. If only COX-2 is inhibited by COX-2 specific inhibitors, pain is alleviated without the associated stomach pain |
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The therapeutic index of SPF is 2. Should more modifications be done before it is released to the market? |
More modifications should be done, as the therapeutic index is too low. If an individual takes 2X the therapeutic dose, it can be lethal; the lethality of the drug is extremely high, rendering the drug unsafe for public comsumption |
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You make another modification of SPF and discover that is not binds directly to and activates opioid receptors. What is this an example of? |
An agonist |
