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In enzymology, a L-glutamate oxidase (EC 1.4.3.11) is an enzyme that catalyzes the chemical reaction L-glutamate + O 2 + H 2 O ⇌ {\displaystyle \rightleftharpoons } 2-oxoglutarate + NH 3 + H 2 O 2 The 3 substrates of this enzyme are L-glutamate , O 2 , and H 2 O , whereas its 3 products are 2-oxoglutarate , NH 3 , and H 2 O 2 .
Glutamate is a common and abundant excitatory neurotransmitter in the central nervous system; however, if there is too much glutamate transmission, this can kill or at least damage neurons and has been implicated in many neurological diseases and disorders [37] therefore the balance that NAAG peptidase contributes to is quite important.
Treatment for glycogen storage disease type III may involve a high-protein diet, to facilitate gluconeogenesis. Additionally the individual may need: [2] [1] [10] IV glucose (if oral route is inadvisable) Nutritional specialist; Vitamin D (for osteoporosis/secondary complication) Hepatic transplant (if a complication occurs)
The 2022 American Diabetes Association (ADA) standards of medical care in diabetes include SGLT2 inhibitors as a first line pharmacological therapy for type 2 diabetes (usually together with metformin), specifically in patients with chronic kidney disease, cardiovascular disease or heart failure.
The end product of the glutaminase reaction, glutamate, is a strong inhibitor of the reaction. Changes in glutamate dehydrogenase, which converts glutamate to 2-oxoglutarate and thereby decreases intramitochondrial glutamate levels, are thereby an important regulatory mechanism of glutaminase activity.
Chronic granulomatous disease (CGD), also known as Bridges–Good syndrome, chronic granulomatous disorder, and Quie syndrome, [1] is a diverse group of hereditary diseases in which certain cells of the immune system have difficulty forming the reactive oxygen compounds (most importantly the superoxide radical due to defective phagocyte NADPH oxidase) used to kill certain ingested pathogens. [2]
GLUT1 deficiency syndrome, also known as GLUT1-DS, De Vivo disease or Glucose transporter type 1 deficiency syndrome, is an autosomal dominant genetic metabolic disorder associated with a deficiency of GLUT1, the protein that transports glucose across the blood brain barrier. [1]
Disulfiram is used as a second-line treatment, behind acamprosate and naltrexone, for alcohol dependence. [7]Under normal metabolism, alcohol is broken down in the liver by the enzyme alcohol dehydrogenase to acetaldehyde, which is then converted by the enzyme acetaldehyde dehydrogenase to a harmless acetic acid derivative (acetyl coenzyme A).