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Nathan Goodyear

Glutamate and the glutamate receptor system: a tar... [Int J Geriatr Psychiatry. 2003] ... - 0 views

  • Under certain conditions, glutamate has a toxic action resulting from an activation of specific glutamate receptors, which leads to acute or chronic death of nerve cells.
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    deep, heavy read on glutamate excitotoxicity and neuronal death leading to neurodegenerative disease
Nathan Goodyear

Inhibitors of glutamate release from breast cancer cells; new targets for cancer-induce... - 0 views

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    Glutamate is a growth factor for cancer.  Cells make glutamate from glutamine in the diet.  Increased glutamate is associated with cancer metastasis and increased cancer bone pain.
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

Estrogen attenuates glutamate-induced cell death by inhibiting Ca2+ influx through L-ty... - 0 views

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    Estradiol inhibits glutamate mediated influx of calcium and thus cell death in cell line.  Glutamate, the principle excitatory neurotransmitter, is involved in neurodegeneration through activation of calcium channels.  This study of cell line cultures found that Estradiol inhibits this process.  I question whether this is applicable to both men and women.  Time will tell.
Nathan Goodyear

Glutamic acid - Top 200 Food Sources of Glutamic acid | Top200Foods.com - 0 views

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    Top 200 food sources of Glutamic Acid
Nathan Goodyear

Exercise increases mitochondrial glutamate oxidation in the mouse cerebral cortex - App... - 0 views

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    exercise found to reduce glutamate excitotoxicity in mouse study.
Nathan Goodyear

Pictorial Review of Glutamate Excitotoxicity: Fundamental Concepts for Neuroimaging - 0 views

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    excellent article on the imaging of excitotoxicity.  Glutamate excitotoxicity is a key component in neurodegenerative diseases: Alzheimers, Parkinsons, ALS, MS...
Nathan Goodyear

CNS Spectrums: Inflammation, Glutamate, and Glia in Depression: A Literature Review - 0 views

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    inflammation, glutamate excitotoxicity and depression.  A very nice review of how inflammation can remotely contribute to other arenas of dysfunction, ie. depression.
Nathan Goodyear

Brain glutamine and glutamate levels in patients with liver cirrhosis: assessed by 3.0-... - 0 views

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    Brain glutamic acid originates from glutamine.  Glutamine should be avoided in those with excitotoxic diseases.
Nathan Goodyear

Glutamate release promotes growth of malignant gli... [Nat Med. 2001] - PubMed result - 0 views

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    some tumors, glioblastoma multiforme, secrete glutamate, which increases aggressive nature of cancer
Nathan Goodyear

Creatine supplementation lowers brain glutamate levels in Huntington's disease. - PubMe... - 0 views

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    Creatine helpful in decreasing glutamate levels in Huntington's disease.
Nathan Goodyear

Glutamate and its receptors in cancer - 0 views

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    Glutamate, a common food additive that enhances flavor, is a growth factor for cancer.  
Nathan Goodyear

Ascorbate inhibits edema in brain slices. | Mendeley - 0 views

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    vitamin C shown to reduce brain edema associated with glutamate excitotoxicity
Nathan Goodyear

Is administrating branched-chain amino acid-enriched nutrition achieved symptom-free in... - 0 views

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    BCAA improve NH3 metabolism.  This is via muscle metabolism as reported in other studies.  This study highlighted the differences in BCAA supplementation.  One caveat is that high glutamine is the result from glutamate and this can increase hepatic encephalopathy.
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

Neurodegenerative disorders: clues from glutamate ... [Crit Rev Neurobiol. 1996] - PubM... - 0 views

  • glutamate antagonists or agents that improve energy metabolism may slow the degenerative process and offer a therapeutic approach for temporarily retarding the progression of these disabling disorders.
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    Magnesium and Zinc improve neurodegenerative disease via glutamate blockade; Poor energy production at foundation of neurodegenerative disease
Nathan Goodyear

[Role of glutamate and excitotoxicity in neurologi... [Rev Neurol (Paris). 1996] - PubM... - 0 views

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    nice abstract on the basic physiologic role of glutamate excitotoxicity
Nathan Goodyear

Pictorial Review of Glutamate Excitotoxicity: Fundamental Concepts for Neuroimaging -- ... - 0 views

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    Very heavy, but good read on glutamate excitotoxicity
Nathan Goodyear

Untitled Page - 0 views

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    review of inflammation, glutamic acid, glial activation and depression
Nathan Goodyear

Inborn-like errors of metabolism are determinants of breast cancer risk, clinical respo... - 0 views

  • We now recognize that human cancers evolve in an environment of metabolic stress. Rapidly proliferating tumor cells deprived of adequate oxygen, nutrients, hormones and growth factors up-regulate pathways that address these deficiencies to overcome hypoxia (HIF), vascular insufficiency (VEGF), growth factor deprivation (EGFR, HER2) and the loss of hormonal support (ER, PR, AR) all to enhance survival and proliferation
  • RAS, PI3K, TP53 and MYC
  • The results suggest that breast cancer could be preceded by systemic subclinical disturbances in glucose-insulin homeostasis characterized by mild, likely asymptomatic, IEM-like biochemical changes
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  • The process would include variable periods of hyperinsulinemia with the consequent systemic MYC activation of glycolysis, glutaminolysis, structural lipidogenesis and further exacerbation of hypoglycemia, the result of MYC's known role as an inhibitor of liver gluconeogenesis
  • The metabolic changes we describe in breast cancer arise in concert with IEM-like changes in oxidative phosphorylation as detected by increased values of the ratio lactate/pyruvate (Supplementary Table 2A, 2B) characteristic of Ox/Phos deficiency [25]. In our study, 76% (70/92) of the European breast cancer patients had lactate/pyruvate ratios values higher than the normal value of 25.8
  • four-fold higher frequency of cancer (including breast) in patients with energy metabolism disorders
  • growing recognition that cancer cells differ from their normal counterparts in their use of nutrients, synthesis of biomolecules and generation of energy
  • glutamine concentrations in the cancer patients were reduced to nearly 1/8 of the levels observed in the normal population
  • blood concentrations of aspartate (p = 1.7e-67, FDR = 8.3e-67) (Figure ​(Figure1E)1E) and glutamate (p = 6.4e-96, FDR = 6.2e-95) (Figure ​(Figure1F)1F) were nearly 10 fold higher than the normal ranges of 0–5 μM/L and 40 μM/L, respectively
  • glutamine consumption associated with parallel increases in glutamate and aspartate (Figure ​(Figure1A1A red arrows) is considered a hallmark of MYC-driven “glutaminolysis”
  • Gln/Glu ratio inversely correlates with i- late stage metabolic syndrome and with ii- increased chance of death
  • changes in glutamine consumption, reflected by the Gln/Glu ratio could provide a metabolic link between breast cancer initiation and diabetes, reflective of a systemic metabolic reprogramming from glucose to glutamine as the preferred source of precursors for biosynthetic reactions and cellular energy
  • lower Gln/Glu ratios inversely correlated with insulin resistance and the risk of diabetes
  • the metabolic dependencies of cancer characterized by excessive glycolysis, glutaminolysis and malignant lipidogenesis, previously considered a consequence of local tumor DNA aberration [23] could, instead, represent a systemic biochemical aberration that predates and very likely promotes tumorigenesis
  • these metabolic disturbances would be expected to remain extant after therapeutic interventions
  • accumulation of very long chain acylcarnitines such as C14:1-OH (p = 0.0, FDR = 0.0), C16 (p = 0.0, FDR = 0.0), C18 (p = 0.0, FDR = 0.0) and C18:1 (p = 1.73e-322, FDR = 1.16-321) and lipids containing VLCFA (lysoPC a C28:0) (p = 1.14-e95, FDR = 1.65e-95) in the blood of breast and colon cancer patients
  • Among the most powerful metabolic equations for MYC-activation is that which links the widely used MYC-driven desaturation marker ratio of SFA/MUFA to the MYC glutaminolysis-associated ratio of (Asp/Gln)
  • liver dysfunction shares many features with both IEM and cancer suggesting a role for hepatic dysfunction in carcinogenesis
  • cancer “conscripts” the human genome to meet its needs under conditions of systemic metabolic stress
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    Breast cancer is a metabolic disease.  Now, where have I heard that cancer is a metabolic disease?
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