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Synaptosomal uptake of alpha-ketoglutarate and glutamine in thioacetamide-induced hepatic encephalopathy in rats

J Albrecht¹, J Waskiewicz, M Dolinska

¹Department of Neurotoxicology, Medical Research Centre, Polish Academy of Sciences, Warsaw.

Metabolic Brain Disease

|February 25, 1998

Abstract:

The kinetics of uptake of two astroglia-derived glutamate (GLU) precursors, alpha-ketoglutarate (alpha-KG) and glutamine (GLN) were determined in synaptosomes derived from rats with acute hepatic encephalopathy (HE) induced with a hepatotoxin, thioacetamide (TAA). TAA treatment increased by 33% Vmax for high affinity, low capacity alpha-KG uptake, without influencing its Km. The increase of the uptake capacity for alpha-KG may represent a response of the GLUergic nerve terminals to the decreased cerebral alpha-KG content, which during HE is associated with depressed activity of pyruvate carboxylase, an enzyme that replenishes alpha-KG in astrocytes. The result is thus consistent with the notion that HE affects the astroglial control of GLUergic neurotransmission. The Km and Vmax for the low affinity, high capacity GLN uptake was not affected by TAA treatment.

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Hepatic Encephalopathy

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...

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