chapter17&18.docx

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Department
Molecular, Cellular and Developmental Biology
Course Code
MCDB 310
Professor
Kenneth Balazovich

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 Making NADH is important because it can go to the ETC to make ATP  Fatty acids can also be degraded to make FADH and NADH o they will also turn into acetyl-CoA and again make more NADH o acetyl-CoA can go into the Krebs cycle  complete degradation of glucose  Look at figure 16.15  All those words mean the same thing  glyceral and three fatty acids make this molecule o these fatty acids can now be degraded o glycerol can be degraded  goes into glycolysis  The products are used as electron transporters  Three fatty acids carry a lot of oxidative power o ester linkages o very non-polar so they are relatively inert and you need a solvation layer around it o solvation layer for lipid droplets = huge energy savings  Fatty aicds are good form of storage energy because carbons are almost completely reduced o (it can be oxidized more) o way higher energy yield than carbs  This is in order of mass without water o the most energy will come from fat o the least is glucose!  Hierarchy of catabolism (what is used first, then next, then last) o basically the reverse of this list o we would use glucose in fluids first (available glucose) o after that other sugars o then you go to glycogen stores (mostly liver, some in muscle) o once that is used up, you move to fats (burned rapidly and easily mobilized  take a lot longer to burn but very large energy store of them) o then you degrade protein to remain alive  One hydration layer around the whole droplet o fatty acids can be compactly stored and are easily available to the enzymes that will break them down in the cytoplasm  Cows bred for certain fat content but they are very fit metabolically  Most fat is stored around arteries – you need a way to mobilize fats to the liver to break it down  Amount of enzyme is going down – store it because you aren’t using it  Usually synthesized in the liver and then transported elsewhere  Lipases = lipoprotein, not phospholases  Some lipase activity in an acidic environment, then some lipase activity in a basic environment o both breaking down fatty acids  Bile salts from from cholesterol o important for digestion in basic environment  Fats just being broken down then transported  In intestine you have those four things o you busted up some fatty acids to get the di and mono or plain glycerol o fatty acids and glycerols can get through, but the di can’t get through (into the intestine layers)  Gets converted back into triglycerides so they can be transported (after they get through layer)  Lipoprotein lipases will break off the fatty acids o Then neutralization, then basic environment in the small intestine o breaking off fatty acids again with lipases here  Fatty acids diffuse across intestine wall o then get made back into triglycerides o those go in the center of the micelle o proteins from the intestine wall will act as ligands o then they float around in the bloodstream and reach receptors (liver, adipose, muscle, etc) o when it gets to receptor, they start opening up, triglycerides come across again into the new organ  Have to bust them down again to get them across the new cell wall they want to enter into o then we decide if we want energy (kreb cycle) or to store (as lipid droplet/triglycerides)  The VLDL is less dense than the LDL because of what’s on the surface and what’s inside  Vascular system and the lymphatic system will both transport them  Lipases are on the outside of the blood cells but facing inside of bloodstream o break down the fatty acids so they can come across the membrane o then can be degraded  We are trying to get to mitochondrial matrix o this part of the cell lets us do fatty acid degradation o into cytoplasm, then across two more membranes to get to the matrix  These are bad for you – make plack on the blood wall o ten fatty acids per molecule of serum albumin  Any remnants can go to liver o any excess fats go to liver to get used  Diabetes  body is reacting exactly as it should but it has improper signaling from insulin o mixed signals makes your body produces ketone bodies o place to store excess acetyl-CoA o serve as extra energy source for CNS  But messed up metabolism (diabetes) will convert fatty acids into ketone bodies (useful form of energy)  Stored fat/glucose are signals o glucose mobilized to make acetyl-CoA o this stuff gets activated to make acetyl-CoA o both get dumped into Krebs cycle  No we have glycerol laying around and we can use it o this is in adipose tissue – can be used in glycolysis in the liver and muscle (a little kidney too)  You need to know this pathway o glycerol kinase phosphorylates glycerol o glycerol 3-phosphate dehydrogenase (NOT glyceraldehyde) o we produce NADH from the dehydrogenase o dihydroxyacetone phosphate is not used in glycolysis but triose phosphate isomerase was  Fatty acids in serum albumin  Glycolysis is the stage 2 box  The stage 1 pox starts with palmitate (16 carbons) o all going to be turned into acetyl-CoA  make 8 acetyl-CoA  They all go into Krebs cycle to make a lot of NADH and FADH o then go to the respiratory chain to get ATP  Oxidative phosphorylation means we have to redox the NADH and FADH o that will cause the phosphorylation of ADP  Beta-oxidation pathway is one of several fatty acid oxidation o break beta to gamma bond to make acetyl-CoA  All the pathways make all three things though o FADH = 1.5 ATP o NADH = 2.5 ATP  So one acteyl-CoA can give you how many ATP? o acetyl-CoA goes into Krebs  3 NADH and 1 FADH o so every acetyl-CoA gives you about 10 ATP  Fatty acids can’t just go through oxidation pathways  not enough reductive potential o so we have to activate them o we put on Coenzyme A  Now it is a very powerful molecule o you need some potential though  you need ATP  This is not what’s really going on though… o the reaction mechanism that produces AMP and 2 Pi o not hydrolysis because you would only get out 1 Pi o adenylylation is a transfer of ADP and you get AMP  that’s the correct answer  Remember you break off a pyrophosphoryl group to get AMP and then can get 19 more kJ energy  Activation via adenylylation o synthetase means it uses ATP  AMP is now added o as a result the pyrophosphatase will break up the pryophasphate and give you an extra 19 kJ  Now add the Coenzyme A o overall we get a -15 delta G  This transporter will stop the cycle o its an antiport, carnitine one way, aceyl-carnitine the other way  We have acetyl-CoA o this system will make aceyl-carnitine to go across o fatty acid with Co-A  enzyme in the membrane (blue thing) puts carnitine onto the fatty acid o that can go through the transporter in exchange for carnitine  Active system for getting the acyl-chain inside o reverse the reaction with carnitine tansferase II o this one take the carnitine off and puts new Co-A on  now this can be degraded  Highly regulated because we don’t want a futile cycle o in the matrix is fatty acid catabolism, don’t want this happening at same time as fatty acid synthesis  The number I enzyme is the regulation step for the transporter *** o malylyl Co-A binds to it to shut it off o when fatty acids are being made this gets bound to the enzyme to shut down transporter  Now we can finally break these things down o even number of carbons fully saturated or with some double bonds o or odd number of carbons without without double bonds  Four steps that are repeated  reduction  NADH or FADH has to be made – dehydrogenation (memorize the enzyme)  transfers 2H+ and 2e- to make FADH  three different isozymes for this  recognize different chain lengths  Making a double bond here o send FADH to the ETC (already have 1.5 ATP)  Need to see where this is happening o start of ETC in this picture o the red guy is a complex of proteins that will use NADH  Next guy is the Krebs cycle enzyme  The guy all the way at the bottom is the one we just talked about o has to have a protein to bind to  prosthetic group  Fatty acids and their degradation goes directly into ETC  First step was reduce the double bond, this one will get rid of the double bond by adding water with a hydratase o The Co-A stays on there to provide energy  DON’T HAVE TO KNOW THE INTERMEDIATE NAMES o doesn’t matter what you start with – you always use the same enzymes  You have to know the generic names of the intermediates, not the specific ones though  Now we are transferring a hydride from the hydroxy-acyl-CoA o now we are producing a NADH o can go to the ETC to make 2.5 ATP  We get another double bond now  Beta oxidation vs. CAC o first step make FADH o then reduce something to make NADH  Flavin then a nicotinamide in the left o in Krebs you flavin to nicotinamide again o only way the reaction to proceed  The fourth step is when you make acetyl-CoA o you are transferring the acetyl group, not the CoA o the coenzyme A is already there, need a second one  you keep breaking off acetyl-CoA to break down the whole 16 carbon chain into little guys  you have to have an activated fatty acid  This is 7 rounds NOT 8 (last rounds just busts it in half)  How many ATP can I get out of the sugar I’m degrading? o we need 7 of everything because there are 7 rounds o we get 8 acetyl-CoA  Oxygen is the finally electron acceptor o we are making a bunch of donors at the top  Hibernating animals produce water by breaking down fats  In the citric acid cycle you use the 8 acetyl-CoA  get 24 NADH and 8 FADH and 8 GTP o turn all of this into ATP  So overall we get 80 ATP  Depending on aerobic vs. anaerobic we make different amounts o 106 to 108 ATP can be made  Activation of fatty acid took an ATP o so if you have to activate a fatty acid, then from the total you have to subtract one ATP o the second ATP is not actually an ATP – the carnitine transporter has to have a gradient set up o the number of kJ is approximately the same to set up the transporter is almost an ATP  If you have acetyl-CoA in the mitochondria matrix already you get 108 o if you have it in cytosol and have to move into it, you get 106  Enoyl-CoA hydratase is the second step o can’t happen if there is more than one double bond  have to get rid of them o doesn’t matter where the double bond is  Undergo beta-oxidation until get to double bond o enzyme comes in and isomerizes the double bond from a cis to a trans if it needs to o the trans double bond is the same kind of double bond in the first step of beta-oxidation  So now can go into second step of beta-oxidation o even number of carbons with either one or no double bond now understood  Now there are multiple double bonds o hydratase will freakout o the isomerase from last slide
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