From NuGOwiki
The NuGOwiki Metabolite Database is a joint initiative of NuGO and HMDB
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| L-Glutamic acid | |
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| Chemical Name | 2-aminopentanedioic acid |
| Chemical Formula | C5H9NO4 |
| CAS Number | 56-86-0 |
| Chemical Information | HMDB00148 |
| Biochemical Taxonomy |
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| Functional Taxonomy | Not Available |
| Nutritional Taxonomy | Not Available |
| Metabolic Pathways |
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| Biofluid Location |
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| Tissue Location |
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| Normal Biofluid Concentrations |
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| Normal Tissue Concentrations | Not Available |
| Diseases / Conditions Related to Nutrition |
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| Other (Monogenic Disorders) | Not Available |
| Abnormal Biofluid Concentrations |
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| Abnormal Tissue Concentrations | Not Available |
| Physiological Processes | Not Available |
| Authors: | |
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Contents |
Introduction
guidelines
Glutamic acid (Glu), also referred to as glutamate (the anion), is one of the 20 proteinogenic amino acids. It is not among the essential amino acids. Glutamate is a key molecule in cellular metabolism. In humans, dietary proteins are broken down by digestion into amino acids, which serves as metabolic fuel or other functional roles in the body. Glutamate is the most abundant fast excitatory neurotransmitter in the mammalian nervous system. At chemical synapses, glutamate is stored in vesicles. Nerve impulses trigger release of glutamate from the pre-synaptic cell. In the opposing post-synaptic cell, glutamate receptors, such as the NMDA receptor, bind glutamate and are activated. Because of its role in synaptic plasticity, it is believed that glutamic acid is involved in cognitive functions like learning and memory in the brain. Glutamate transporters are found in neuronal and glial membranes. They rapidly remove glutamate from the extracellular space. In brain injury or disease, they can work in reverse and excess glutamate can accumulate outside cells. This process causes calcium ions to enter cells via NMDA receptor channels, leading to neuronal damage and eventual cell death, and is called excitotoxicity. The mechanisms of cell death include: * Damage to mitochondria from excessively high intracellular Ca2+. * Glu/Ca2+-mediated promotion of transcription factors for pro-apoptotic genes, or downregulation of transcription factors for anti-apoptotic genes. Excitotoxicity due to glutamate occurs as part of the ischemic cascade and is associated with stroke and diseases like amyotrophic lateral sclerosis, lathyrism, and Alzheimer's disease. glutamic acid has been implicated in epileptic seizures. Microinjection of glutamic acid into neurons produces spontaneous depolarization around one second apart, and this firing pattern is similar to what is known as paroxysmal depolarizing shift in epileptic attacks. This change in the resting membrane potential at seizure foci could cause spontaneous opening of voltage activated calcium channels, leading to glutamic acid release and further depolarization. (http://en.wikipedia.org/wiki/Glutamic_acid)
Biological Function
Catabolism
Diseases / Conditions Related to Nutrition
- Acute seizures
- Anoxia
- Juvenile myoclonic epilepsy (JME)
- Nondiabetic patients with Chronic Heart Failure
- Probable Alzheimer's Disease
- Refractory localization-related epilepsy (RLE)
- Schizophrenia
- Schizophrenia (Men)
- leukemia
- leukemia with CNS disease
Other (Monogenic) Disorders