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  1. #1
    Twincities MN kuan's Avatar
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    If you're glycogen depleted and don't eat after working out

    Does your body turn fat into glycogen and store it in your liver and muscles?

  2. #2
    Killing Rabbits
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    No. Small amounts of protein turn to glycogen, but no fat.

  3. #3
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    Quote Originally Posted by kuan
    Does your body turn fat into glycogen and store it in your liver and muscles?
    Enthalpic is right. Your body tears down your muscle to renew the glycogen.

    Probably not the result that you were looking for...
    Eric

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  4. #4
    Senior Member DannoXYZ's Avatar
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    Quote Originally Posted by kuan
    Does your body turn fat into glycogen and store it in your liver and muscles?
    Fat cannot be converted into glucose then glycogen. Fats are only broken apart in the fatty-acid spiral into Acetyl-CoA which is used to feed the Krebs Cycle to generate ATP.

    The glucose that's used to replenish glycogen then comes from ingested carbs or from existing muscle proteins through gluconeogenesis.

    Some articles about nutrition and muscle-building. Note these are bodybuilders and notice the ratios of their nutrition:

    Bodybuilding.com - Anabolic Ammunition Arsenal (look about 3/4 down page for calorie-mix calculator)
    ABCbodybuilding - A Scientific Investigation into the Rationality of Post Workout Carbohydrate Consumption
    ABCbodybuilding - Analysis of Nutrient use during Low, Moderate, and High Intensity Exercise
    SparkNotes - Functions of Carbohydrates
    Peak Performance - How much protein do athletes need? note "up to 150gm a day" for performance athletes.
    Last edited by DannoXYZ; 01-29-07 at 11:08 PM.

  5. #5
    Twincities MN kuan's Avatar
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    Danno, yes or no and SIMPLE explanation would work. OK actually that was just about right for me.

    OK thanks everyone.

  6. #6
    Eternal Cat3 Rookie branman1986's Avatar
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    I love learning esoteric information like that Keep it up Danno/Eric!

    We've got such a large forum base here, that we've got experts in a lot of different fields...might as well learn something from 'em

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    Senior Member DannoXYZ's Avatar
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    Quote Originally Posted by kuan
    Danno, yes or no and SIMPLE explanation would work. OK actually that was just about right for me.

    OK thanks everyone.
    figured you got the simple answer already, so I gave you a little more detail on why. Have fun and keep up the good work!

    Here's how the two suppliers of raw-materials for glycogen-replenishment works:

    carbs (glucose,fructose) -> glucose-6-phosphate -> glycogen

    tissue-protein -> nitrogen-pool -> pyruvic-acid -> glucose-6-phosphate -> glycogen

    Notice that the protein pathway is more complicated and slower. So during recovery with available glucose, that's used preferentially to proteins, thus sparing your muscles from catabolism.

    The ingested proteins in the typically 4:1 carb-protein mix actually serves a different purpose. It actually causes a higher insulin-response than carbs alone and speeds transport of glucose into the muscles for quicker glycogen-replenishment.
    Last edited by DannoXYZ; 01-30-07 at 07:27 AM.

  8. #8
    Senior Member Richard Cranium's Avatar
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    tissue-protein -> nitrogen-pool -> pyruvic-acid -> glucose-6-phosphate -> glycogen
    Yeah, and what's missing is the fact that some glucose is necessary for direct metabolic support of the central nervous system. Therefore, if and when some one severely depletes their glycogen levels, the body will start sending "shut down" signals warning the brain that blood-glucose levels are not being maintained.

    I've still never found out what it is about nerve cells, that require glucose. Nor have I ever discovered what percentage of the basal metabolic requirements have to be met by glucose.

    If you could calculate the caloric value of remaining liver glycogen and knew the basal metabolic glucose requirements of a given person, you could predict the longest period they could safely fast. (take that you pro-anne nut jobs)

  9. #9
    Isaias NoRacer's Avatar
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    Quote Originally Posted by Richard Cranium
    Yeah, and what's missing is the fact that some glucose is necessary for direct metabolic support of the central nervous system. Therefore, if and when some one severely depletes their glycogen levels, the body will start sending "shut down" signals warning the brain that blood-glucose levels are not being maintained.

    I've still never found out what it is about nerve cells, that require glucose. Nor have I ever discovered what percentage of the basal metabolic requirements have to be met by glucose.

    If you could calculate the caloric value of remaining liver glycogen and knew the basal metabolic glucose requirements of a given person, you could predict the longest period they could safely fast. (take that you pro-anne nut jobs)
    Not entirely true about shutdown messages, because of ketone bodies:

    Quote Originally Posted by Effect of ketone body infusion on plasma catecholamine and substrate concentrations during acute hypoglycemia in man - L Frolund, H Kehlet, NJ Christensen and KG Alberti

    Experimental studies have shown that ketone body infusion inhibits the catecholamine response to hypoglycemia. We have studied six men during insulin-induced hypoglycemia who were concomitantly infused with saline or 3-hydroxybutyrate at dose rates of 4 and 13 mg/kg.min. The mean blood concentrations of 3-hydroxybutyrate increased to about 0.45 and 3 mmol/liter, respectively. The results show that the glucose response to insulin; hypoglycemic symptoms; and the adrenaline, noradrenaline, and cortisol responses to hypoglycemia were not influenced by ketone infusion at any dose rate.
    Quote Originally Posted by Role of glucose and ketone bodies in the metabolic control of experimental brain cancer - Seyfried TN, Sanderson TM, El-Abbadi MM, McGowan R, Mukherjee P. Biology Department, Boston College, Chestnut Hill, MA 02467, USA. thomas.seyfried @ bc.edu

    Brain tumours lack metabolic versatility and are dependent largely on glucose for energy. This contrasts with normal brain tissue that can derive energy from both glucose and ketone bodies. We examined for the first time the potential efficacy of dietary therapies that reduce plasma glucose and elevate ketone bodies in the CT-2A syngeneic malignant mouse astrocytoma. C57BL/6J mice were fed either a standard diet unrestricted (SD-UR), a ketogenic diet unrestricted (KD-UR), the SD restricted to 40% (SD-R), or the KD restricted to 40% of the control standard diet (KD-R). Body weights, tumour weights, plasma glucose, beta-hydroxybutyrate (beta-OHB), and insulin-like growth factor 1 (IGF-1) were measured 13 days after tumour implantation. CT-2A growth was rapid in both the SD-UR and KD-UR groups, but was significantly reduced in both the SD-R and KD-R groups by about 80%. The results indicate that plasma glucose predicts CT-2A growth and that growth is dependent more on the amount than on the origin of dietary calories. Also, restriction of either diet significantly reduced the plasma levels of IGF-1, a biomarker for angiogenesis and tumour progression. Owing to a dependence on plasma glucose, IGF-1 was also predictive of CT-2A growth. Ketone bodies are proposed to reduce stromal inflammatory activities, while providing normal brain cells with a nonglycolytic high-energy substrate. Our results in a mouse astrocytoma suggest that malignant brain tumours are potentially manageable with dietary therapies that reduce glucose and elevate ketone bodies.

    PMID: 14520474 [PubMed - indexed for MEDLINE]
    Quote Originally Posted by Enzymes of Ketone Body Utilization in Human Tissues: Protein and Messenger RNA Levels of Succinyl-Coenzyme A (CoA):3-Ketoacid CoA Transferase and Mitochondrial and Cytosolic Acetoacetyl-CoA Thiolases - FUKAO, TOSHIYUKI; SONG, XIANG-QIAN; MITCHELL, GRANT A.; YAMAGUCHI, SEIJI; SUKEGAWA, KAZUKO; OR, TADAO II; KONDO, NAOMI
    ...
    Ketone bodies are important vectors of energy transfer(1). Ketogenesis primarily occurs in liver. The relative capacities of tissues for ketone body utilization is thought to be determined by their levels of ketolytic enzymes. Ketosis is a normal physiologic response to fasting and other stresses by which fat-derived energy is provided to extrahepatic tissues, particularly brain, which has no other non-glucose-derived source of energy.
    ...
    Last edited by NoRacer; 01-30-07 at 09:14 AM.
    2009 mileage = 14,738 miles; 2010 mileage = 15,234 miles; 2011 mileage = 17,344 miles; 2012 mileage = 11,414 miles; 2013 = 12,169

  10. #10
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    Quote Originally Posted by Richard Cranium
    Yeah, and what's missing is the fact that some glucose is necessary for direct metabolic support of the central nervous system. Therefore, if and when some one severely depletes their glycogen levels, the body will start sending "shut down" signals warning the brain that blood-glucose levels are not being maintained.

    I've still never found out what it is about nerve cells, that require glucose. Nor have I ever discovered what percentage of the basal metabolic requirements have to be met by glucose.

    If you could calculate the caloric value of remaining liver glycogen and knew the basal metabolic glucose requirements of a given person, you could predict the longest period they could safely fast. (take that you pro-anne nut jobs)

    Initially your body will tear down muscle to supply glucose to the body. It does this by the use of diabetogenic hormones like cortisol, epenephrine and glucagon. In a state of starvation the CNS will switch over to using ketones as its main source of fuel when the liver can no longer supply glucose via gluconeogenesis. The CNS will demand that it receives a certain amount of glucose, but when it does not it will use ketones to operate, as will muscles. The small intestine is not able to run on ketones, it can only use glutamate and glucose. If you are starving yourself there is probably no need for your small intestine to function as it normally does.

    The interesting thing about nerve cells is that they do not need insulin to absorb glucose as does most of the bodies other cells, and this is why prolonged hyperglycemia can cause so many problems, especially retinopathy, as well as other neuropathies. The retina has the most biologically active nervous tissue by weight than almost any other part of the body.

    In the average 70Kg male the liver is able to store about 300 calories worth of glycogen, and about 600 in the muscles. The muscles can export only a very minute amount of glucose for the rest of the body because the enzyme glucose 6 phosphatase is not present or present in only very small amounts in the muscle, but is present within hepatocytes.

  11. #11
    Killing Rabbits
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    Quote Originally Posted by Richard Cranium
    I've still never found out what it is about nerve cells, that require glucose.

    I’ve heard it’s because the axon can be quite long and reach large distances from the cell body. Other fuel substrates cannot diffuse sufficiently to feed the terminal ends.

  12. #12
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    Quote Originally Posted by DannoXYZ
    Fat cannot be converted into glucose then glycogen. Fats are only broken apart in the fatty-acid spiral into Acetyl-CoA which is used to feed the Krebs Cycle to generate ATP.
    Fat is composed of fatty acids ester bonded to a glycerol. If you claim that fat can't be made into glucose, how come glycerol is used in gluconeogenis?

    If you wish I can try to post the whole article.

    Dietary supplementation with n-3 fatty acids increases gluconeogenesis from glycerol but not hepatic glucose production in patients with non- insulin-dependent diabetes mellitus
    I Puhakainen, I Ahola and H Yki-Jarvinen
    Second Department of Medicine, University of Helsinki, Finland.

    Fish-oil supplementation decreases serum triacylglycerols but may worsen hyperglycemia in patients with non-insulin-dependent diabetes mellitus. The reason for the possible deterioration of glycemia is unclear. We examined whether inhibition of triacylglycerol synthesis by n-3 fatty acids changes lipolysis, glycerol gluconeogenesis, or fatty acid oxidation. Nine obese patients with non-insulin-dependent diabetes mellitus participated in a randomized double-blind crossover study in which 6 wk of n-3 fatty acid supplementation (12 g fish oil) was compared with 6 wk of corn plus olive oil. Serum triacylglycerols decreased by 30% during n-3 fatty acid supplementation. Glycerol gluconeogenesis ([U-14C]glycerol) increased by 32%. However, overall glucose production ([3-3H]glucose), glycemic control, and fatty acid oxidation remained unchanged. Thus, 6 wk of n-3 fatty acid supplementation lowers triacylglycerols in patients with non-insulin- dependent diabetes mellitus without worsening glycemic control. However, n-3 fatty acid supplementation increases glycerol gluconeogenesis, which could contribute to deterioration of glycemic control during long-term treatment with high doses of fish-oil supplements

    And how about

    Glycerol Metabolism

    The predominant source of glycerol is adipose tissue. This molecule is the backbone for the triacylglycerols. Following release of the fatty acid portions of triacylglycerols the glycerol backbone is transported to the liver where it it phosphorylated by glycerol kinase yielding glycerol-3-phosphate. Glycerol-3-phosphate is oxidized to DHAP by glycerol-3-phosphate dehydrogenase. DHAP then enters the glycolytic if the liver cell needs energy. However, the more likely fate of glycerol is to enter the gluconeogenesis pathway in order for the liver to produce glucose for use by the rest of the body.

  13. #13
    Senior Member DannoXYZ's Avatar
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    Quote Originally Posted by !!Comatoa$ted
    Fat is composed of fatty acids ester bonded to a glycerol. If you claim that fat can't be made into glucose, how come glycerol is used in gluconeogenis?

    If you wish I can try to post the whole article.


    And how about

    Glycerol Metabolism
    Check this out: IndState.edu - Gluconeogenesis. The pathway is the important part, not the components. Just because something is made up of similar parts, doesn't mean it goes through the same pathway. Like fructose vs. glucose, they're all made up of CHO, but the pathway is vastly different on how they're metabolized. The 3-carbon glycerol backbone is tiny compared to the 48 or 54-carbon fatty-acid chains.

    "Oxidation of fatty acids yields enormous amounts of energy on a molar basis, however, the carbons of the fatty acids cannot be utilized for net synthesis of glucose. The two carbon unit of acetyl-CoA derived from b-oxidation of fatty acids can be incorporated into the TCA cycle, however, during the TCA cycle two carbons are lost as CO2. Thus, explaining why fatty acids do not undergo net conversion to carbohydrate."
    The fatty-acid spiral cleaves off pieces of the chain and makes AcetylCoA. At no point is the fatty-acid converted to glucose. However, the small glycerol backbone can be converted to glucose, but it's a tiny fraction of the total energy generated from fatty-acids.

    Last edited by DannoXYZ; 01-31-07 at 02:45 AM.

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    Quote Originally Posted by DannoXYZ
    Check this out: IndState.edu - Gluconeogenesis. The pathway is the important part, not the components. Just because something is made up of similar parts, doesn't mean it goes through the same pathway. Like fructose vs. glucose, they're all made up of CHO, but the pathway is vastly different on how they're metabolized. The 3-carbon glycerol backbone is tiny compared to the 48 or 54-carbon fatty-acid chains.



    The fatty-acid spiral cleaves off pieces of the chain and makes AcetylCoA. At no point is the fatty-acid converted to glucose. However, the small glycerol backbone can be converted to glucose, but it's a tiny fraction of the total energy generated from fatty-acids.

    Thank you for your wonderful diagrams.

    I see what you are saying that the fats themselves are not made into glucose, but lipids can be used to make glucose, the lipid supplies the glycerol, which is a very important part of lipids. But using your logic one could say that lipids do not make acetyl co-a because the whole lipid is not used only the fatty acid minus the glycerol, and bodily fat, adipose, is made up of more than just fatty acids. The fact is part of the fat (aka triglycerides) is used to make glucose, so saying glucose cannot be made from stored fat does not seem accurate, since a portion of the lipid can be used to make glucose. Just like a portion of the lipid is used to make ketones, and acetyl co-a.

    And as your nice diagram shows it is a fatty acid spiral, in order for this to happen it seems that you need to separate fatty acids from the glycerol in able to utilise the fatty acids in the spiral. What happens to the glycerol. As a result of the breakdown of lipids glycerol is used to make glucose via gluconeogenesis can be made now how can it be that lipids are not able to increase glucose in the blood, just as glucose in the blood can increase fat. In the gluconeogenic pathway glycerol is used in the pathway to make glucose.

    If you have some nice diagrams of gluconeogenesis, take a look at them, what part of lipids do you see being used to make it?
    Last edited by !!Comatoa$ted; 01-31-07 at 02:28 PM.

  15. #15
    Killing Rabbits
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    Even with short chain fatty acids the molecular weight of a triglyceride will be >800g/mol. The molar mass of glycerol is 92g/mol and yields 4.3kcal/g as food energy.

    You can see that one gram of dietary fat will contain equal to or less than 0.1g of glycerol (1 x 92/800+), working out to be about 0.4kcal/g of “carb energy” per gram of fat. With fat providing about 9kcal/g, a whopping 4.5% of that could come from the glycerol. So to reload the muscles with carbs the body would have to burn a prohibitive amount of fatty acids to liberate enough glycerol. Furthermore, your body doesn’t like to burn glycerol at all unless starving; it prefers to keep the glycerol inside the cells for the next incoming free fatty acid to attach to.

  16. #16
    Oil it! sfrider's Avatar
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    Quote Originally Posted by !!Comatoa$ted
    The fact is part of the fat (aka triglycerides) is used to make glucose, so saying glucose cannot be made from stored fat does not seem accurate, since a portion of the lipid can be used to make glucose.
    One triglyceride consisting of 18-carbon fatty acids produces 139 molecules of ATP from the fatty acids and 9 molecules of ATP from the glycerol. Only the glycerol pathway, via the peruvic acid precursor or oxaloacetic acid can synthesize glycogen/glucose. (For those who aren't familiar with this, human fatty acids are 14-22 carbon, with 16 and 18 being most common. They're always even carbon counts because of how they're made.) Not sure what determines where the glycerol ends up (glucose or ATP), perhaps the presence/absence of CO2? Or NH3 blocking some enzymatic activity (like creation of peruvic acid)? Just because there happens to be a pathway for glycogen synthesis from glycerol, it's not a foregone conclusion that just because the CNS needs glucose that fat catabolism will produce it...

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    Oil it! sfrider's Avatar
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    To answer the original question, fat synthesis is one-way; we can turn fatty acids to ATP, but not back to glycogen. Which accounts for why it's so bloody difficult to lose fat; if our bodies had any significant ability to turn it back into glycogen we'd lose it as quickly as we gained it. Our bodies are also extremely efficient at turning glycogen into fat, basically our adipose tissues can absorb it as fast as we can digest it.

  18. #18
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    Quote Originally Posted by sfrider
    One triglyceride consisting of 18-carbon fatty acids produces 139 molecules of ATP from the fatty acids and 9 molecules of ATP from the glycerol. Only the glycerol pathway, via the peruvic acid precursor or oxaloacetic acid can synthesize glycogen/glucose. (For those who aren't familiar with this, human fatty acids are 14-22 carbon, with 16 and 18 being most common. They're always even carbon counts because of how they're made.) Not sure what determines where the glycerol ends up (glucose or ATP), perhaps the presence/absence of CO2? Or NH3 blocking some enzymatic activity (like creation of peruvic acid)? Just because there happens to be a pathway for glycogen synthesis from glycerol, it's not a foregone conclusion that just because the CNS needs glucose that fat catabolism will produce it...
    Thank you for the explanation.

    I understand that the body does not usually obtain glucose from lipids, and when it does it is a very small amount, and pyruvate can be used to make glucose. To make glycogen from glycerol seems like the body would use a tremendous amount of energy, and in context to the OP I am sure that fat stores will not prevent proteins from being disassembled. I only wished to point out that lipids can be used to form glucose, and not that lipids are a major source of glucose. Even some of the people that have said it is in no way shape or form possible to make glucose from lipids have also indicated that there is a possibility for them to be made from glycerol, which is an integral part of lipids. This is all I wished to point out. I also believe that fatty acids do not form glucose, but to liberate the tremendous energy stored in lipids the glycerol is freed from the fatty acids, and then the glycerol may be used to form glucose. As well, the contribution of glycerol to form glucose is very limited but still exists.

    This stuff interests me a great deal, and I have learned a lot from Danno et al, and I am not trying to be-little any one. I only wish to challenge views that are contradictory to what I have learned, and take part in a discussion in a subject that I am interested in, nothing more.

    Again, thank you all I have learned a great deal from many forum members and have had my passion for biology fueled by reading many of the intelligent posts here, even if mine are not always so.

  19. #19
    Senior Member Richard Cranium's Avatar
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    Screw it, reformat your posts - you've ff-ed up the thread too much to bother reading.

  20. #20
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    Quote Originally Posted by Richard Cranium
    Screw it, reformat your posts - you've ff-ed up the thread too much to bother reading.

    I find reding through mozilla it is screwd up, but IE it is just fine. Or maybe it is a plot against you?

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