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Hepatic [2-13C]acetate metabolism by jirds infected with Echinococcus multilocularis

Published online by Cambridge University Press:  11 April 2024

J. Schoen
Affiliation:
Department of Biology, University of Winnipeg, Winnipeg, Manitoba, Canada R3B 2E9
M. Novak*
Affiliation:
Department of Biology, University of Winnipeg, Winnipeg, Manitoba, Canada R3B 2E9
B.J. Blackburn
Affiliation:
Department of Chemistry, University of Winnipeg, Winnipeg, Manitoba, Canada R3B 2E9
*
*Author for correspondence. Fax: (204) 783 7981 E-mail: mnovak@uwinnipeg.ca

Abstract

Carbon-13 decoupled 1H spin echo NMR spectroscopy, with and without population inversion, was used to study carbon flow between the host, Meriones unguiculatus, and the parasite, Echinococcus multilocularis. This was accomplished by monitoring [2-13C]acetate metabolism in the liver of jirds infected with metacestodes of this parasite. Thirty minutes after injection of labelled acetate solution into the portal vein, 13C enrichment was observed in hepatic acetate, β–hydroxybutyrate, succinate, alanine, lactate and glucose. For E. multilocularis cysts, at this time,13C enrichment was observed in the same metabolites as in livers and, in addition, citrate. At 120 min there was a significant decrease in the amount of label present in all hepatic metabolites whereas more label was found in the majority of the parasite metabolites. The results confirm that exogenous acetate, through randomization of the 13C in biochemical pathways of host liver, ends up in hepatic glucose. As this biosynthetic route is not available to the parasite, the presence of 13C enriched glucose in the cysts clearly indicates that the parasite is siphoning off glucose that is newly synthesized by the host. At 120 min some of this labelled glucose was stored in parasite glycogen whereas some of it had been catabolized to succinate, alanine, lactate and acetate, end products which are excreted back into the host.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1999

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