info to all- how arginine citrulline malate akg others -kerb cycle

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    info to all- how arginine citrulline malate akg others -kerb cycle


    http://www.lionden.com/muscle_animations.htm
    http://www.people.virginia.edu/~rjh9u/krebs.html
    http://www.johnkyrk.com/krebs.html
    http://web.indstate.edu/thcme/mwkin...metabolism.html
    http://users.rcn.com/jkimball.ma.ul.../UreaCycle.html
    http://www.stjude.org/faculty/0,251...30_4131,00.html
    http://www.bmb.leeds.ac.uk/illingwo...tabol/krebs.htm

    learn more about the kerbs cycle , and how most of the stuff conver to urea and ammonium, and more nitrogen matabolism , then you'll find arginine and citrulline products mostly thrown out of the body and not very helpfull especially if you eat alot of protein , plus arginine or citrulline + anything like malate or alpha keto glutarate is used in the cycle for energy so arginine alone will do the job as it was used in most of the research to raise nitric oxide, and for energy you might get the same results from eating malic acid alone or akg alone, mostly other products in the kerbs cycle might be used for this option as they convert or release nadh nad pyruvate and atp, and might be seen soon in the supplement industry , so know your stuff before you buy

    Aslo read this from : http://web.indstate.edu/thcme/mwkin...metabolism.html

    "Urea Cycle Defects (UCDs)

    A complete lack of any one of the enzymes of the urea cycle will result in death shortly after birth. However, deficiencies in each of the enzymes of the urea cycle, including N-acetylglutamate synthase, have been identified. These disorders are referred to as urea cycle disorders or UCDs. More information on the individual UCDs can be found in the Inborn Errors in Metabolism pages. A common thread to most UCDs is hyperammonemia leading to ammonia intoxication with the consequences described below. Deficiencies in arginase do not lead to symptomatic hyperammonemia as severe or as commonly as in the other UCDs.
    Clinical symptoms are most severe when the UCD is at the level of carbamoyl phosphate synthetase I. Symptoms of UCDs usually arise at birth and encompass, ataxia, convulsions, lethargy, poor feeding and eventually coma and death if not recognized and treated properly. In fact, the mortality rate is 100% for UCDs that are left undiagnosed. Several UCDs manifest with late-onset such as in adulthood. In these cases the symptoms are hyperactivity, hepatomegaly and an avoidance of high protein foods.
    In general, the treatment of UCDs has as common elements the reduction of protein in the diet, removal of excess ammonia and replacement of intermediates missing from the urea cycle. Administration of levulose reduces ammonia through its action of acidifying the colon. Bacteria metabolize levulose to acidic byproducts which then promotes excretion of ammonia in the feces as ammonium ions, NH4+. Antibiotics can be administered to kill intestinal ammonia producing bacteria. Sodium benzoate and sodium phenylbutyrate can be administered to covalently bind glycine (forming hippurate) and glutamine (forming phenylacetylglutamine), respectively. These latter compounds, which contain the ammonia nitrogen, are excreted in the feces.

    Dietary supplementation with arginine or citrulline can increase the rate of urea production in certain UCDs.


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    Table of UCDs

    UCD Enzyme Deficiency Symptoms/Comments
    Type I Hyperammonemia Carbamoylphosphate synthetase I with 24h - 72h after birth infant becomes lethargic, needs stimulation to feed, vomiting, increasing lethargy, hypothermia and hyperventilation; without measurement of serum ammonia levels and appropriate intervention infant will die: treament with arginine which activates N-acetylglutamate synthetase
    N-acetylglutamate synthetase Deficiency N-acetylglutamate synthetase severe hyperammonemia, mild hyperammonemia associated with deep coma, acidosis, recurrent diarrhea, ataxia, hypoglycemia, hyperornithinemia: treatment includes administration of carbamoyl glutamate to activate CPS I
    Type 2 Hyperammonemia Ornithine transcarbamoylase most commonly occurring UCD, only X-linked UCD, ammonia and amino acids elevated in serum, increased serum orotic acid due to mitochondrial carbamoylphosphate entering cytosol and being incorporated into pyrimidine nucleotides which leads to excess production and consequently excess catabolic products: treat with high carbohydrate, low protein diet, ammonia detoxification with sodium phenylacetate or sodium benzoate
    Classic Citrullinemia Argininosuccinate synthetase episodic hyperammonemia, vomiting, lethargy, ataxia, siezures, eventual coma: treat with arginine administration to enhance citrulline excretion, also with sodium benzoate for ammonia detoxification
    Argininosuccinic aciduria Argininosuccinate lyase
    (argininosuccinase) episodic symptoms similar to classic citrullinemia, elevated plasma and cerebral spinal fluid argininosuccinate: treat with arginine and sodium benzoate
    Hyperargininemia Arginase rare UCD, progressive spastic quadriplegia and mental retardation, ammonia and arginine high in cerebral spinal fluid and serum, arginine, lysine and ornithine high in urine: treatment includes diet of essential amino acids excluding arginine, low protein diet"

    from this site scroll in between and read about nitrogen balance so you'll understand more:

    " Unlike fats and carbohydrates, nitrogen has no designated storage depots in the body. Since the half-life of many proteins is short (on the order of hours), insufficient dietary quantities of even one amino acid can quickly limit the synthesis and lower the body levels of many essential proteins. The result of limited synthesis and normal rates of protein degradation is that the balance of nitrogen intake and nitrogen excretion is rapidly and significantly altered. Normal, healthy adults are generally in nitrogen balance, with intake and excretion being very well matched. Young growing children, adults recovering from major illness, and pregnant women are often in positive nitrogen balance. Their intake of nitrogen exceeds their loss as net protein synthesis proceeds. When more nitrogen is excreted than is incorporated into the body, an individual is in negative nitrogen balance. Insufficient quantities of even one essential amino acid is adequate to turn an otherwise normal individual into one with a negative nitrogen balance.
    The biological value of dietary proteins is related to the extent to which they provide all the necessary amino acids. Proteins of animal origin generally have a high biological value; plant proteins have a wide range of values from almost none to quite high. In general, plant proteins are deficient in lysine, methionine, and tryptophan and are much less concentrated and less digestible than animal proteins. The absence of lysine in low-grade cereal proteins, used as a dietary mainstay in many underdeveloped countries, leads to an inability to synthesize protein (because of missing essential amino acids) and ultimately to a syndrome known as kwashiorkor, common among children in these countries. "

    so in conclusion save your money and buy protein, and don't throw it on no products

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    never been a fan but tried the basic AKG powder from vitaplus (100 grams for 8.95). Seems to help with vascularity, a little with strength and definetly voluminization. Might try it again.

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