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Nathan Goodyear

Branched-chain amino acids increase arterial blood ammonia in spite of enhanced intrins... - 0 views

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    Good review of the effects of BCAA on ammonia metabolism.  BCAA increase intramuscular NH3 production through the production of alpha-ketoglutarate.
Nathan Goodyear

Branched-chain amino acids and ammonia metabolism in liver disease: Therapeutic implica... - 0 views

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    BCAA are low in patients with liver cirrhosis due to increased glutamate production from glutamine.  The addition of BCAA in these patients is not without side effects--increased NH3 production.  The addition of alpha ketoglutarate should alleviate this risk.
Nathan Goodyear

Glioblastoma Cells Require Glutamate Dehydrogenase to Survive Impairments of Glucose Me... - 0 views

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    This article describes how important glutamine is as an alternative energy source in Glioblastoma. Cancer is a substrate-level dependent energy production disease. If one disrupts glycolysis as a source of energy, then many cancers will use glutamine through glutaminolysis. The cancer cells will do this through glutamate dehydrogenase and glutamate production. This will increase alpha-ketoglutarate which will then feed the substrate-level phosphorylation through the TCA cycle. This study mentioned that EGCG is a way to naturally inhibit glutamate dehydrogenase.
Nathan Goodyear

Amino acid management in cancer - 0 views

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    Serine, glycine, glutamine, glutamate, asparagine upregulated in cancer. Most glutamine is converted to glutamate to drive alpha-ketoglutarate production to drive energy production. It also upregulates mTOR signaling.
Nathan Goodyear

We're Not "DON" Yet: Optimal Dosing and Prodrug Delivery of 6-Diazo-5-oxo-L-norleucine ... - 0 views

  • Glutamine is the most abundant amino acid in blood
  • Rapidly proliferating healthy cells (GI epithelium, lymphocytes) or cells under physiologic stress have increased demand for glutamine
  • Glutamine is transported into cells by one of multiple amino acid transporters (e.g. ASCT2, BOAT2), several of which are thought to be upregulated in cancer cells
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  • it is hydrolyzed to glutamate and ammonia by glutaminase (‘glutaminolysis’)
  • Glutamate, produced from glutamine by glutaminase and glutamine amidotransferase activities, may be further metabolized to alpha ketoglutarate and provide a carbon skeleton source for the mitochondrial tricarboxylic acid cycle (TCA cycle)
  • Glutamine-derived glutamate is also involved in the synthesis of the reducing equivalent glutathione, vital to maintaining cellular redox status
  • Many tumors become largely dependent on glutamine to provide carbon and nitrogen building blocks needed for proliferation
  • In cancer model systems, Eagle and colleagues first demonstrated tumor cells in culture require supplementation with exogenous glutamine for efficient proliferation
  • It was subsequently shown that when deprived of glutamine tumor cells undergo apoptosis
  • The most well-characterized oncogene to regulate glutamine metabolism is MYC (9), which enhances glutaminase expression, upregulates glutamine transporters, and enhances glutamine utilization in energy production and biosynthesis
  • Other pro-tumorigenic regulators such as KRAS and mTOR, as well as tumor suppressors (p53, VHL) have also been associated with alterations in glutamine metabolism
  • Tumor cells are highly adaptable and alter nutrient uptake and metabolic networks to resist single agent glutaminase inhibition
  • cells in the microenvironment of several tumor types upregulate glutamine production, thereby enabling tumor cells to escape glutaminase inhibition
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