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PPP and Glycogen

Discussion in 'The Epi-Paleo Diet' started by QiGuy1997, Feb 17, 2014.

  1. QiGuy1997

    QiGuy1997 New Member

    I've seen Doctor Kruse mention that D-Ribose and the PPP are good at refilling glycogen levels in the liver. Now, if this is true, it means that the stress hormones that are claimed to be mobilized in response to low blood-sugar/glycogen during ketosis would not actually be produced. However, I can't find anything related to the PPP or Ribose refilling liver glycogen. Could anyone either provide me with the biochemical pathways by which the PPP synthesizes glycogen or, if not, a source/citation/study showing a connection between the PPP and synthesis of glycogen?
  2. Josh

    Josh New Member


    Attached Files:

  3. Jonathin

    Jonathin Gold Member

    I don't think that Jack has said that ribose makes glycogen. In EMF4 he does say that 'D-ribose restores glycogen levels' which I admit could be seen as a bit confusing. But if you look at


    that does not make sense. It seems that ribose can make abundant ATP so that glucose and fructose are not needed to quick recycle meager ATP reserves to maintain energy output. The is the main point of EMF4.

    Glycerol from the breakdown of fats converts to glyceraldehyde-3-P (G3P) which according to


    in PPP III clearly shows that G3P can convert to ribose through a couple of intermediates. High sugar or high NADPH inhibits the frontend of the PPP from glucose-6-P. Yes, fructose can also use Pathway III but there are other issues regarding abundant fructose. It also seems the G3P can do a reverse glycolysis path and form glycogen as well. I believe this is what he is talking about.
  4. QiGuy1997

    QiGuy1997 New Member

    I do see that G3P can be converted to ribose in the PPP. However, something you must notice is this pathway produces no NADPH. So yes, the fats on the epi-paleo diet can produce ribose but not NADPH, nullifying must of the benefits of the PPP in the first place. If you want to produce lots of NADPH, you have to run the PPP on glucose and fructose. There is no other pathway for producing NADPH (regenerating glutathione) through the PPP than glucose/fructose. Your body can't do it with fat.
  5. Jonathin

    Jonathin Gold Member

    G3P can make ribose &, through conversion to fructose6P and glucose6P, NADPH . You need to look more closely at the pathways that I provided. Seems like you don't want to see what is there. Also protein degrades to carbs and can supply glycolysis pathway and be diverted to PPP. Lots of carbs tends to inhibit PPP. Read all the cites in EMF4. I don't feel like there is a big debate about this. If people were not make NADPH on a low carb diet they would be showing obvious degradation of hormone and glutathione function. This is conformational.
    Jack Kruse likes this.
  6. Jack Kruse

    Jack Kruse Administrator

    The key is understanding the G3Pdh shuttle in out mitochondria is a major redox switch. If you look in EE12 I posted a pic of the redox potentials from NADH to O2. Study it. It is critical. You guys all think life is based upon pathways in books that do not use the redox potential in that pic. It is now clear mitochondria can both foward and reverse their flow in ETC. This means the redox potential is the controller of how this works. I have strung many blogs together and am painting you a picture of how the PPP works in cold ketosis and hydrated state. It appears that glycerol-3-Pdh is critcal protectant against electron and proton overload from any source in mitochondria. It protects us by inducing insulin resistance. When you have high blood sugars married with high exogenous insulin or fructose consumption from a bad diet to induce physiologic insulin resistance you need to have mitochondrial G3Pdh for effective reverse electron flow through complex I to generate mandatory superoxide/H2O2 for mitochondrial signaling.

    So when thinking about ETC, you need to forget pathways and and look at redox potentials of the cytochromes and the inner mitochondrial membrane. Think about blog What powers life and death here. Now this implies we need to grouping inputs to the ETC by their redox potential rather than physical location on the inner mitochondrial membrane. We know that carbs feed NADH at cytochrome one and Fats go to cytochrome 2. When the redox potential changes at the cytochrome.............this is what determines how a mitochondria works. Not a pathway. It is the charges of all electron donors from any source. They carry energy, information, and spin data for the cytochromes and the redox potential is key determining feature of where things go.
    All mitochondrial NADH inputs are through complex I at -280mV ( see the pic in EE12) and these electrons flow from here towards the positive potential of +600mV, provided by oxygen at complex IV. This is normal function. QiGuy and many opthers think this is how it always happens because that is what the text book says. Wrong. Here is why: To do work to animate life, pumping protons can also be done to set up the delta psi in mitochondria. This high delta psi can be "burned as free heat" when needed. High delta psi happens with insulin and low delta psi happens in insulin resistance of any cause. With evolution, mammals did this to stay warm in freezing cold underground holes. This is why we can do it.
    For insulin to peoperly signal you need to have an elevated delta psi which allows a nano-molar pulses of H2O2 to cripple a phosphatase that is in the insulin pathway to allow for proper insulin/receptor complex signalling. Cold also inactivates this pathway. Think CT 6. You dont need insulin in winter when no carbs are around. Moreover, insulin does not work well below 62 degree F. See Gilbert Ling.
    This implies we have the ability to uncouple using insulin.............normally. See the oprah blog post. Without the ability to uncoupling, the process become quite energy efficient and energy from the electron is largely conserved by our redox potential in the mitochondria. In this way we can harvest the power of the photoelectric effect without any energy cost. Think zero entropy.

    The interesting point is that mitochondrial G3Pdh inputs electrons to the CoEnQ couples in cytochromes for electron tunneling which has a redox potential of +20mV.
    So with respect to mitochondrial G3Pdh, it is taking a cytoplasmic NADH, which could theoretically be shuttled to the mitochondrial matrix, and hence to complex I, at -280mV, and inputting it to the ETC at +20mV. The energy lost by skipping from -280mV to +20mV would normally pump four protons to generate heat.
    After a glucose load any oxidation of the abnormally elevated FFAs of insulin resistant people still provides a continuous +20mV input using ETF dehydrogenase's FADH2 acting on the CoQ couple, which is ultimately derived from the FADH2 of the first step of beta oxidation, ie it's FADH2 transporting electrons all the way, there is no energy wastage when using fats to limit insulin's action. In the absence of these inappropriate FFAs, the correct way to reduce the CoQ couple is using mtG3Pdh which shuts down insulin's action at the cost of generating heat because it uses NADH, stepped down to FADH2, as a direct input at the CoQ level. We want a reduced the CoQ couple when there is metabolic oversupply as a reduced CoQ couple allows reverse electron flow through complex I and insulin resistance. Insulin resistance, via reverse electron flow through complex I, is what is wanted, heat is a by-product.

    What if that elevated FFA level was maintained long term, say if you are eating a ketogenic template? Remember FFA bring the mitochondria tons of protons.........and a lot of lower energy electrons from fat and protein.

    As adipocytes become progressively more resistant to the the anti-lipolytic effect of insulin (another aspect not material now), plasma free fatty acids rise even under levels of insulin which should be suppressing them. This is a paradox or mismatch. Unless these free fatty acids are converted to CoA derivatives they will DIRECTLY uncouple respiration themselves. This should reduce delta psi while increase metabolic rate. This is precisely what a polar bear does in winter. We should be doing it to but we cant...............when our redox potential is shot. (or a lost metabolic flexibility, due to reduced to the level of delta psi and superoxide. think T2D)

    A reduced delta psi will not support reverse electron flow through complex I!!!!!! Here is where a lowered redox hurts. The essential insulin induced pulse of superoxide that is converted to H2O2, will not occur. Mitochondrial signaling is then BROKEN. There will be fasting insulin resistance. This paper spelled it out. http://www.ncbi.nlm.nih.gov/pubmed/23730255

    The insulin signalling cascade is tonically restrained by a phosphatase which deactivates the insulin/receptor complex (which activates itself by auto-phosphorylation: Think about what I said in EE 11 now............) as soon as the process begins or tries too. You need a warm climate or warm adapted mammal and carbs for this to happen. For insulin to signal you need to have an elevated delta psi which allows a nanomolar pulse of H2O2 to cripple this phosphatase and so allow the insulin/receptor complex to get signalling.

    With reduced delta psi this isn't going to happen. We have enhanced insulin resistance of starvation until the time when food arrives. Sound familiar to how winter should work to anyone?

    You can increase delta psi to get insulin working when you are a mammal who controls their own environment. This is the story of EMF 4. As soon as we have access to glycolysis combined with beta oxidation we have the possibility to generate marked reverse electron flow through complex I and re-inhibit the action of insulin using much greater generation of H2O2 than is needed for insulin's initial activation. Metabolically, the mitochondria do this at this time to stop caloric overload in any individual cell, by diverting excess calories to storage in adipocytes. From the NADH:FADH2 ratio, long chain saturated fats do this best. Monounsaturates appear to be designed to allow a normal combination of glucose and fatty acid oxidation and PUFA fail to generate adequate insulin resistance to protect an individual fat cell from an overload of metabolic substrate.
    Now do not get me wrong.........I don't think life is as simple as "ketones by-pass complex I". In fact they provide almost as much NADH (complex I only) per unit FADH (bypasses complex I) as glucose. They are acetyl CoA precursors, some provide extra NADH to acetyl CoA, some don't. So we are not by-passing complex I. FADH (cytochrome 2) is the only route to bypass complex I. In Complex II electron tunnels through iron-sulfur protein clusters (PMID: 16780790).
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  7. Jack Kruse

    Jack Kruse Administrator

    Palmitate is a partial by-pass but is not a fuel in the CNS. Glycerol-3-dehydrogenase (the key shuttle that Qiguy is missing in his understanding) is also an FADH generator that links the PPP to FATS in COLD. G3Pdh is active depending upon the redox potential present from the environmental signaling, not just from fructose or glucose loads found in metabolic pathways of biochem books.
    But what is special about ketones is that they drop the voltage across the inner mitochondrial membrane without compromising ATP generation. So proteins can still unfold with a lower redox potential. They also push redox chemistry in the cytoplasm to maximize the energy release per ATP molecule hydrolyzed by using water chemistry. "Structure water" with redox cofactors was found to accelerate electron transfer (PMID: 16311331) So ketosis provides full ATP energy yield (147 vs 36 ATP) without the need for insulin action (which does need an intact complex I to work ideally) on the electron transport chain. The low membrane voltage during ketosis also limits free radical production at complex I, which may has a significant protective effect limiting excessive cell damage when a lowered redox state is the norm due to neolithic disease.
    Increasing delta psi requires increased electrons density or energies (think summer time electron energies being higher than winter electrons) in to the respiratory chain through complex I. In the blunted insulin signalling situation with a low delta psi and low redox we can't use GLUT4 transporters. This is how the Maxwell demon cytochromes tell seasons PEOPLE. However, we can, get the mitochondrial signal at cytochrome one when we generate a high enough plasma glucose levels, get sufficient glucose in to the cell to generate enough of a delta psi to allow the pulse of H2O2 and its downstream mitochondrial signaling effects to occur. So we clearly can overcome the inability of insulin to signal in the presence of FFAs......this is a winter and starvation program built in to our mitochondria. How do we do it?

    The cost is that an elevated blood glucose level is needed. This is why people have higher blood glucose when they switch fuels or when they have metabolic syndrome. They need to generate a signal for biogenesis. In T2D once the cytochrome one is shot..........you lose the ability to make new mitochondria and then ROS builds and your redox potential lowers disease ensues and death comes faster from all comers. This is why ,many docs look at with the ratio of fasting glucose to fasting insulin, called the HOMA score. It turns out an elevated HOMA score is a marker of UNCOUPLING at the delta psi level in mitochondria. It should be associated with an increased metabolic rate in proportion to the degree of fatty acid induced uncoupling. When it is not we know the mitochondria are BUSTED.
    Himms-Hagen have suggested that FFAs stimulate UCP-1 and UCP-3 expression too. Here we are back to oprah blog post..........We do not need free T3 in cold because eNOS can help us uncouple. BOOM.

    1. http://www.ncbi.nlm.nih.gov/pubmed/24024165
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  8. yewwei.tan

    yewwei.tan Gold

    Thanks for the great posts Jack. It tied together lots of stuff I've been recently reading on your's and Peter's blogs.

    In case anyone is interested, Petro Dobromylskyj (Peter) from Hyperlipid wrote about this topic in some of the posts of his great protons series:

    - Discussing uncoupling and insulin resistance -- http://high-fat-nutrition.blogspot.com/2013/11/protons-30-uncoupling-and-metabolic.html
    - FADH2:NADH ratios and MUFA. Note the magic 0.47 ratio -- http://high-fat-nutrition.blogspot.com/2012/08/protons-fadh2nadh-ratios-and-mufa.html
    - Knocking out G3P in mice -- http://high-fat-nutrition.blogspot.com/2013/12/protons-33-mtg3pdh-knockout-mice_29.html

    You must read the comments on all of those posts as well.

    This also gets me re-thinking my weird experiences with MCTs that I just talked about in my log: http://forum.jackkruse.com/index.php?threads/take-it-slow.9428/page-3#post-111338
  9. QiGuy1997

    QiGuy1997 New Member

    Thanks for all the information between the three of you! Jonathin, I decided to take your advice and read all the cites on EMF 4 and, if anything, I am now more confused. Only about 3-4' of the cites had to do with the PPP. The very first cite showed me that, in rats at least, a high fat diet altered eating patterns, caused weight gain and decreased the PPP function. The next showed that DHEA is a pretty potent inhibitor of the PPP. The last one relating to the PPP did, in fact show that high glucose inhibits the PPP. However, blood sugar commonly rises on a ketogenic due to increased insulin resistance. Hmm. If anything, this suggests to lower DHEA levels and increase insulin sensitivity in order to clear glucose faster, right? I've yet to see any evidence that a high-fat/ketogenic diet helps one "enter" the PPP and I haven't seen any real evidence that a moderate carb diet reduces the PPP. If you have any studies on this, or evidence in this regard, I would greatly appreciate it.
  10. Jack Kruse

    Jack Kruse Administrator

    Electrons make the world go round........I told you we are designed to collect a lot of them........now let me help you understand the secret of the key to life. It opens many gates. The temp and cytokine level and charge determines the fate of the electron:

    Magnetic fields are very hard to localize in proteins........so how do they take their chaos and make them scalable for a cell? Consider that if you’re trying to create tiny magnetic bits on a nanowire, collagen, water or a track, the magnetic fields from the electromagnets used to read and write data tend to spread out, making it difficult to prevent interaction with adjacent strips, especially as devices get smaller and smaller.

    What if I tell you we can stop this magnetic spread with a simple action? We can now stop magnetic domains on demand simply by toggling the applied voltage. Think the redox potential is a small issue?

    Remember human membranes ARE fat and generate/store electron charge. Sulfated proteins attach to these saturated fats and produce voltage! Now you know why. Everything is important at a molecular level in 3 D.

    Lady evolution built a new type of device that controls magnetism in much the same way that a transistor controls a flow of electricity. The key ingredient is a layer of ion-rich material in which atoms have been stripped of electrons, leaving them with an electric charge. You might begin to look at mitochondria and collagen differently. Think about what happens to water next to collagen......charge separates into H3O+ and -OH. H30 has its electrons stripped. Water surrounds proteins......when ATP is present. What does ATP do? ATP strips electrons from proteins...........it is electron withdrawing.

    If electrons are stripped from atoms to form an electric current, why doesn't the atomic/molecular structure of the material from which they are stripped change you ask?

    So what happens when something happens to remove electrons from semiconductors?

    Removing electrons from an atom is called ionization. Even though an electron is stripped from atom, its mass is not changed since electrons have no mass. Electrons however, have a negative charge. This charge is under infinite control of the electromagnetic force. Of course, when electrons are stripped from atom or proteins it becomes more positively charged than it was before since it lost an electron. ATP is electron withdrawing protein, (Gilbert Ling) so its goal is to strip electrons to make proteins more positively charged. This makes them very reactive to the electromagnetic force because this force only acts on charged particles. Re read EE11. So the atomic structure of proteins remains identical to a biology textbook metabolic pathways but difference comes in how negatively or positively charged an atom actually is. This is why all neurodegenerative diseases are more sensitive to the electromagnetic force and why they are all associated with low levels of ATP and abnormal protein folding.

    The brain is normally loaded with lipid like cholesterol. Cholesterol and collagen are semiconductors and when they are stripped of electrons they lose energy, information, and spin. This is why memory declines when they decline chronically. Now think about why cholesterol is in the brain's lipid membranes and all cell membranes?
    A small voltage applied to a small electrode above this thin layer (Think Becker's DC current or the current in CSF) can either attract or repel those ions; the ions, in turn, can directly modify the properties of an underlying magnet and halt the flow of magnetic domains. This could lead to a new family of “magneto-ionic” devices that can do some amazing things. Think February 2014 webinar.......or think about the magnetico. Think quasicystalline functions.

    The effect depends on chemical interactions at the boundary between thin layers of "magnetic materials" (water and collagen) and solid-state electrolyte materials that are sandwiched together (think white matter tracts in the brain or in nerves). When you understand this type of solid state physics it becomes obvious it’s really the interfacial chemistry that determines the magnetic properties of matter. Where is the DC current? Interfascial water below myelin and outside the axon.

    Theoretically in practice, such a system would use a "wire (collagen) or strip of ferromagnetic material ( cytochromes/blood/metallproteins) with a series of regularly spaced, small electrodes on top of it. The magnetic bits between these electrodes can then be selectively written or read to form information or memory.

    What is special about this physics? Once the orientation of the magnetic bit between two electrodes has been set by this device (think unipolar magnetico or the native magnetic field), it inherently will retain its direction and position (spintronics from redox rx or Feb 2014 webinar) even in the absence of power. So, in practice, you could set a magnetic bit, then turn the power off until you need to read it back (sleep and memories). This memory is built in to your mitochondria, collagen, and nerve cells over time. You collect the data and wisdom of subatomic particles to sharpen your senses with time with the information contained in these particles.

    Because the magnetic switching requires no magnetic field, there is next to no energy dissipation in this arrangement........sound zero entropy no?
    Understanding the detailed origins of these effects could allow the creation of simple, low-power information-technology devices.......sounds a lot like how a cell works huh?
    Last edited: Feb 20, 2014
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  11. Jack Kruse

    Jack Kruse Administrator

    The origin of steroid hormones in mammals is cholesterol that is metabolized by the mitochondrial CYP11A1 system. The cytochrome P450 is fed with reduction equivalents via a small electron transfer chain consisting of NADPH, adrenodoxin reductase, and adrenodoxin. These reductive components are all made when the mammal is stepped in the PPP. Though the redox behavior of the individual protein components has been studied previously, the kinetics of the system in its entirety has not yet been worked out.
    But lets consider these facts:
    Linoleic acids are necessary to build mitochondrial membranes and specifically transfer charge. Coconut oil, pig lard, duck fat and beef tallow resist breakdown at frying temps.

    Linoleic acid (LA) is an unsaturated omega-6 fatty acid. It is a colorless liquid at room temperature. In physiological literature, it has a lipid number of 18:2 cis,cis-9,12. Chemically, linoleic acid is a carboxylic acid with an 18-carbon chain and two cis double bonds; the first double bond is located at the sixth carbon from the methyl end.

    Linoleic acid belongs to one of the two families of essential fatty acids. The body cannot synthesize linoleic acid from other food components. So we got to have it.
    Remember human brains and membranes ARE fat and generate/store electron charge. Sulfated proteins attach to these saturated fats and produce voltage! BOOM

    Cholesterol is a necessary fat that only causes trouble when oxidized and electron hungry. Context you wont get from a metabolic pathway. Follow the electron not the pathway.
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  12. Jack Kruse

    Jack Kruse Administrator

    WHILE BIOLOGY FOCUSES on subtle differences in various life forms, simple chemistry shouts commonality. And the common instrument is conducted by quantum mechanics on a molecular level
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  13. Jack Kruse

    Jack Kruse Administrator

    Abundant electron supplies keep us healthy and occasional oxidative bursts and pH shifts address problems.

    Electron sharing and exchange is the ultimate boy-girl thing at the atomic level, the energetic currency of the material world!
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  14. Josh

    Josh New Member

    Thank you for this explanation, it is illuminating and cool.....I feel the elegant functional simplicity of the system is beginning to emerge.
  15. QiGuy1997

    QiGuy1997 New Member

    I fully see the importance of electrons and the PPP in health. However, I have seen no evidence proving or even suggesting that a high-fat, ketogenic diet increases the PPP or allows us to enter it. I haven't seen a single study or metabolic pathway diagram to suggest this. If I'm missing a study or a simple pathway which connects increased PPP to a ketogenic diet, could you point me in the right direction?
    Also, with the regards to the concept that saturated/unsaturated fats compose the cell membrane, I'm rather skeptical towards that. I think Gilbert Ling's Association Induction hypothesis did an excellent job at proving the cell membrane does not exist, let alone play such crucial roles in physiology.
  16. Jack Kruse

    Jack Kruse Administrator

    Where is happens is the G3Phdh shuttle.......I said that above in detail. You need to go learn about that shuttle.

    Where your confusion comes from is this: the atomic structure of proteins remains identical to a biology textbook metabolic pathways and that is all YOU LEARN.......... but difference comes in how negatively or positively charged an atom actually is and this comes from 3 D molecular atomic rearrangements that are a scale below what is in a text book but is WAY MORE IMPORTANT THAN ANY PATHWAY.
  17. NeilBB

    NeilBB New Member


    Pollack explains that the lipid membranes can still exist and play important roles despite their not being the dogmatically believed impenetrable barrier, and in the absence of the Na K pump, based on Lings AI hypothesis in his earlier book called Cells, Gels, and the Engines of Life.
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  18. Jack Kruse

    Jack Kruse Administrator

    OK lets look here: 3,940,120 youtube hits. Lustig on Fructose. sure moderate fruit in season won't hurt you, but in excess it will destroy your liver. likewise a glass of red wine won't hurt you, but over-indulge and you will kill your liver. Sure, sugars are used in the body, i.e. ribose for RNA etc. But that don't mean you should over-indulge on that stuff. Always remeber seasonality. Eating apples from Chile in winter is like artificial lights at night when it is supposed to be dark. Mis-Match. When you eat does matter.......but to your own N=1 How some one eats in NYC is different than someone in Rural Provence France.
  19. Jack Kruse

    Jack Kruse Administrator

    How the PPP uses cold and fat:The Pentose-phosphate pathway has a wide range of purposes in the cell. It provides a constant supply of NADPH, which is used in biosynthesis. The pathway also produces Ribose-5-phosphate, which is required for nucleic acid synthesis. Also in the Pentose-phosphate pathway two glycolytic intermediates are formed:
    1. Fructose-6-phosphate (the Qiguy/PEAT WAY) and
    2.Glyceraldehyde-3-phosphate. (THE KRUSE WAY VIA FATS)

    Regulation of the Pentose Phosphate Pathway:
    Due to the first step of this pathway being reversible, it is highly regulated. As a result the enzyme Glucose-6-phosphate dehydrogenase is inhibited by NADPH and also by fatty acid esters of coenzyme A.

    Glycerol is a precursor for synthesis of triacylglycerols and of phospholipids in the liver and adipose tissue. When the body uses stored fat as a source of energy, glycerol and fatty acids are released into the bloodstream. In some organisms, the glycerol component can be converted into glucose by the liver and, thus, provide energy for cellular metabolism.
    Before glycerol can enter the pathway of glycolysis or gluconeogenesis (depending on physiological and environmental conditions), it must be converted to their intermediate glyceraldehyde 3-phosphate in the following steps:
    Glycerol To Glycerol kinase To Glycerol-3-phosphate To Glycerol-3-phosphate dehydrogenase To Dihydroxyacetone phosphate To Triosephosphate isomerase To Glyceraldehyde 3-phosphate

    Now the next step.......in understanding:

    FATS STOP THE NEED FOR THE physiologic FRUCTOSE PATH...................What is this tied to? COLD/KETOSIS/HYDRATION of proteins and the activation of Brown fat that liberates fats!!!! Cold empties adipocytes to FFA to make PROTONS for UCP1 and UCP3 to make heat and for the cell to make the reducing elements........need for maintanence of the redox potential. This is tied to sympathetic nervous system response to cold. I spoke about this in CT 6. Any biochem book talks about the shuttle but they do not understand how it shuttles subatomic elements.
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  20. Jack Kruse

    Jack Kruse Administrator

    This glycerol 3 phosphate molecule has a special shuttle that PeataTarians forget. Paleo and Qiguy too. This is a metabolic pathway controlled by transition metal maxwell demons. It allows electrons to skip cytochrome 1. Using it allows cytoplasmic NADH to enter the electron transport chain. Little known area of the PPP is in play here folks...........

    They happen to have two special glycerol 3 phosphate dehydrogenases which make up the shuttle. Free in the cytosol there is cytosolic G3P dehydrogenase, which actually uses NADH to add a pair of hydrogens to a glycolysis intermediate (dihydroxyacetone phosphate) to form G3P directly.

    The other G3P dehydrogenase really does dehydrogenate G3P, back to dihydroxyacetone phosphate. But this second G3P dehydrogenase is embedded in the outer surface of the inner mitochondrial membrane. KEY POINT!!! Anyone guess why? Think what I told you special in the quantum electron blog 2 years ago about FADH2? And it contains an FAD/FADH2 moiety which takes these two hydrogens and uses them to reduce the CoQ couple, feeding electrons in to the electron transport chain. FADH2 is our special fat pathway quantum tunneler......it allows glucose to act like saturated fat when the shuttle is active in cold environments or during starvation.

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