Activation of liver G-6-Pase in response to insulin-induced hypoglycemia or epinephrine infusion in the rat
Autor: | Carine Zitoun, Ludovic Guignot, Isabelle Bady, Gilles Mithieux |
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Rok vydání: | 2002 |
Předmět: |
Male
medicine.medical_specialty Epinephrine Physiology Insulin induced hypoglycemia Endocrinology Diabetes and Metabolism Dexamethasone Rats Sprague-Dawley Physiology (medical) Internal medicine Medicine Animals Insulin G 6 pase Glucocorticoids business.industry Adrenalectomy Hypoglycemia Rats Enzyme Activation Endocrinology Glucose Liver High glucose Glucose-6-Phosphatase business medicine.drug |
Zdroj: | American journal of physiology. Endocrinology and metabolism. 282(4) |
ISSN: | 0193-1849 |
Popis: | This study was conducted to test the hypothesis of the activation of glucose-6-phosphatase (G-6-Pase) in situations where the liver is supposed to sustain high glucose supply, such as during the counterregulatory response to hypoglycemia. Hypoglycemia was induced by insulin infusion in anesthetized rats. Despite hyperinsulinemia, endogenous glucose production (EGP), assessed by [3-3H]glucose tracer dilution, was paradoxically not suppressed in hypoglycemic rats. G-6-Pase activity, assayed in a freeze-clamped liver lobe, was increased by 30% in hypoglycemia ( P < 0.01 vs. saline-infused controls). Infusion of epinephrine (1 μg · kg−1· min−1) in normal rats induced a dramatic 80% increase in EGP and a 60% increase in G-6-Pase activity. In contrast, infusion of dexamethasone had no effect on these parameters. Similar insulin-induced hypoglycemia experiments performed in adrenalectomized rats did not induce any stimulation of G-6-Pase. Infusion of epinephrine in adrenalectomized rats restored a stimulation of G-6-Pase similar to that triggered by hypoglycemia in normal rats. These results strongly suggest that specific activatory mechanisms of G-6-Pase take place and contribute to EGP in situations where the latter is supposed to be sustained. |
Databáze: | OpenAIRE |
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