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J Biol Chem, Vol. 273, Issue 14, 8088-8093, April 3, 1998
From the We have recently cloned the murine
glucagon receptor (GR) gene and shown that it is expressed mainly in
liver. In this organ, the glucagon-GR system is involved in the control
of glucose metabolism as it initiates a cascade of events leading to
release of glucose into the blood stream, which is a main feature in
several physiological and pathological conditions. To better define the
metabolic regulators of GR expression in liver we analyzed GR mRNA
concentration in physiological conditions associating various glucose
metabolic pathways in vivo and in vitro in the
rat and in the mouse. First, we report that the concentration of the GR
mRNA progressively increased from the first day of life to the
adult stage. This effect was abolished when newborn rodents were
fasted. Second, under conditions where intrahepatic glucose metabolism
was active such as during fasting, diabetes, and hyperglycemic clamp,
the concentration of GR mRNA increased independent of the origin of the pathway that generated the glucose flux. These effects were blunted
when hyperglycemia was corrected by phlorizin treatment of diabetic
rats or not sustained during euglycemic clamp.
In accordance with these observations, we demonstrated that the
glycolytic substrates glucose, mannose, and fructose, as well as the
gluconeognic substrates glycerol and dihydroxyacetone, increased the
concentration of GR mRNA in primary cultures of hepatocytes from
fed rats. Glucagon blunted the effect of glucose without being
dominant. The stimulatory effect of those substrates was not mimicked
by the nonmetabolizable carbohydrate L-glucose or the
glucokinase inhibitor glucosamine or when hepatocytes were isolated
from starved rats. In addition, inhibitors of gluconeogenesis and
lipolysis could decrease the concentration of GR mRNA from hepatocytes of starved rats. Combined, these data strongly suggest that
glucose flux in the glycolytic and gluconeogenic pathways at the level
of triose intermediates could control expression of GR mRNA and
participate in controlling its own metabolism.
In Vivo and in Vitro Regulation of
Hepatic Glucagon Receptor mRNA Concentration by Glucose
Metabolism
,
,,,, and
Department of Biochemistry, Albert Einstein
College of Medicine, Bronx, New York 10461 and Centre de
Recherche sur l'Endocrinologie Moléculaire et le
Développement, CNRS, 92190 Meudon-Bellevue, France
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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