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Am J Physiol Endocrinol Metab 268: E965-E973, 1995;
0193-1849/95 $5.00
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AJP - Endocrinology and Metabolism, Vol 268, Issue 5 E965-E973, Copyright © 1995 by American Physiological Society

ARTICLES

Mechanism of gluconeogenesis inhibition in rat hepatocytes isolated after in vivo hypoxia

C. M. Pison, C. Chauvin, E. Fontaine, F. Catelloni, C. Keriel, B. Paramelle and X. M. Leverve
Laboratoire de Therapeutique, Universite Joseph Fourier, Grenoble, France.

Gluconeogenesis was studied in hepatocytes isolated from fasted rats submitted to 24 h of hypoxic exposure (inspired O2 fraction 0.1) or to room air. Hepatocytes from hypoxic rats compared with controls exhibited a lower gluconeogenic rate with lactate (5.1 +/- 0.3 vs. 7.2 +/- 0.3 mumol.min-1.g dry cells-1, P < 0.001) but not with dihydroxyacetone (9.1 +/- 0.3 vs. 9.4 +/- 0.4 mumol.min-1.g dry cells-1), suggesting involvement of the phosphoenolpyruvate-pyruvate cycle. Experiments with perifused hepatocytes from hypoxic and control rats showed a single relationship between phosphoenolpyruvate and glucose flux (JGlc) but two different curves when cytosolic oxalacetate was plotted against JGlc. The decreased phosphoenolpyruvate carboxykinase (PEPCK) activity in the hypoxic group (9.0 +/- 0.9 vs. 16.2 +/- 1.9 nmol.min-1.mg protein-1, P < 001) without change in the Michaelis constant further settled the involvement of this step. The significant decrease in PEPCK mRNA levels in livers from hypoxic rats led us to propose that in vivo hypoxic exposure inhibits gluconeogenesis at the PEPCK level by decreasing PEPCK gene transcription.


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