Pancreas -Insulin

(2) Insulin


Insulin (SR E BP- irresponsive genes


Glucokinase induction PEPCK repression

(3) Insulin



(4) Glucose


Glycogen repletion

Signal metabolite

Insulin/glucose-responsive genes

Insulin/glucose-responsive genes

PEPCK repression G6-Pase induction hepatoma cells and primary cultured hepatocytes; this effect is, at least in part, mediated by a transcriptional mechanism (Argaud et al., 1997). Again, a glucose metabolite seems to be involved in this stimulation since an increase in the concentration of the glycolytic activator fructose-2,6-bisphosphate as well as substrates (xylitol, fructose) entering the glycolytic pathway at different steps mimic the effect of glucose (Argaud et al., 1997; Massillon, 2001). In vivo effects of xylitol on the induction of the glucose-6-phosphatase gene have also been described (Massillon et al., 1998). This was paralleled by a doubling of the concentration ofxylulose-5-phosphate but no change in glucose-6-phosphate concentration.

For all the genes sensitive to both insulin and glucose, both factors do act in synergy either as activators or as inhibitors. This is obviously not the case for the glucose-6-phosphatase gene. The physiological relevance ofthis peculiarity presently is not understood. This could indicate that glucose-6-phosphatase has an as yet unknown function in relation to glucose availibility.

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