NDLI: Energy metabolism in brain cells: effects of elevated ammonia concentrations

Content Provider	Springer Nature Link
Author	Hertz, Leif Kala, Geeta
Copyright Year	2007
Abstract	Both neurons and astrocytes have high rates of glucose utilization and oxidative metabolism. Fully 20% of glucose consumption is used for astrocytic production of glutamate and glutamine, which during intense glutamatergic activity leads to an increase in glutamate content, but at steady state is compensated for by an equally intense oxidation of glutamate. The amounts of ammonia used for glutamine synthesis and liberated during glutamine hydrolysis are large, compared to the additional demand for glutamine synthesis in hyperammonemic animals and patients with hepatic encephalopathy. Nevertheless, elevated ammonia concentrations lead to an increased astrocytic glutamine production and an elevated content of glutamine combined with a decrease in glutamate content, probably mainly in a cytosolic pool needed for normal activity of the malate-asparate shuttle (MAS); another compartment generated by glutamine hydrolysis is increased. As a result of reduced MAS activity the pyruvate/lactate ratio is decreased in astrocytes but not in neurons and decarboxylation of pyruvate to form acetyl coenzyme A is reduced. Elevated ammonia concentrations also inhibit decarboxylation of α-ketoglutarate in the TCA cycle. This effect occurs in both neurons and astrocytes, is unrelated to MAS activity and seen after chronic treatment with ammonia even in the absence of elevated ammonia concentrations.
Starting Page	199
Ending Page	218
Page Count	20
File Format	PDF
ISSN	08857490
Journal	Metabolic Brain Disease
Volume Number	22
Issue Number	3-4
e-ISSN	15737365
Language	English
Publisher	Springer US
Publisher Date	2007-09-20
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	α-Ketoglutarate dehydrogenation Astrocytes Glucose metabolism Glutamate Hepatic encephalopathy Malate-aspartate shuttle Pyruvate carboxylation Pyruvate dehydrogenation Oncology Biochemistry Neurology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Biochemistry Neurology (clinical) Cellular and Molecular Neuroscience

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