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Mechanism of gluconeogenesis inhibition in rat hepatocytes isolated after in vivo hypoxia
Ist Teil von
American journal of physiology: endocrinology and metabolism, 1995-05, Vol.268 (5), p.E965-E973
Ort / Verlag
United States
Erscheinungsjahr
1995
Quelle
MEDLINE
Beschreibungen/Notizen
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.