Ascorbate as a substrate for glycolysis or gluconeogenesis. evidence for an interorgan ascorbate cycle

G. Banheavi, L. Braun, F. Puskâs, M. Csala, J. Mandl

Research output: Contribution to journalArticle

Abstract

Ascorbate catabolism was investigated in murine and human cells unable to synthesize ascorbate due to the missing gulonolactone oxidase activity. In HepG2 cells the addition of ascorbate or dehydroascorbate resulted in high glucose production, while human erythrocytes, MCF7 cells and the cellular elements of the murine blood were able to metabolize ascorbate or dehydroascorbate to lactate. The oxidative agent menadione stimulated, while the transketolase inhibitor oxythiamine inhibited the metabolism of dehydroascorbate in each of these three cell types. Our results suggest that ascorbate breakdown through the pentose phosphate pathway can reach the glycolytic/gluconeogenic route in different cells. In ascorbate synthesizing species the ascorbate-1 a date route in peripheral cells may form a catabolic branch of an interorgan ascorbate cycle, where hepatocytes are responsible for ascorbate synthesis. The catabolic part of this cycle using exogenous ascorbate could be demonstrated even in humans cells.

Original languageEnglish
JournalFASEB Journal
Volume11
Issue number9
Publication statusPublished - 1997

Fingerprint

Gluconeogenesis
gluconeogenesis
glycolysis
Glycolysis
Oxythiamine
Cells
Transketolase
Pentoses
Vitamin K 3
Substrates
Metabolism
Lactic Acid
Oxidoreductases
Blood
Phosphates
cells
Glucose
Pentose Phosphate Pathway
MCF-7 Cells
Hep G2 Cells

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Ascorbate as a substrate for glycolysis or gluconeogenesis. evidence for an interorgan ascorbate cycle. / Banheavi, G.; Braun, L.; Puskâs, F.; Csala, M.; Mandl, J.

In: FASEB Journal, Vol. 11, No. 9, 1997.

Research output: Contribution to journalArticle

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