On the mechanism of diazoxide-induced hyperglycemia

Infusion of diazoxide (16.5 mg./kg. in 10 minutes) into normal unanesthetized dogs resulted in a prompt hyperglycemia due to increased hepatic glucose production as measured with a 3-3H-glucose primer-infusion technique. Plasma insulin and glucagon were decreased. Glucose uptake failed to increase....

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Bibliographic Details
Published inDiabetes (New York, N.Y.) Vol. 26; no. 10; pp. 931 - 935
Main Authors Altszuler, N, Moraru, E, Hampshire, J
Format Journal Article
LanguageEnglish
Published United States 01.10.1977
Subjects
Animals
Blood Glucose - metabolism
Diazoxide
Dogs
Glucagon - blood
Hyperglycemia - blood
Hyperglycemia - chemically induced
Insulin - blood
Phentolamine - pharmacology
Somatostatin - pharmacology
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Summary:Infusion of diazoxide (16.5 mg./kg. in 10 minutes) into normal unanesthetized dogs resulted in a prompt hyperglycemia due to increased hepatic glucose production as measured with a 3-3H-glucose primer-infusion technique. Plasma insulin and glucagon were decreased. Glucose uptake failed to increase. Diazoxide administration during period of alpha adrenergic receptor blockade with phentolamine still caused hyperglycemia and increased glucose production. Glucose uptake was inhibited despite adequate plasma insulin. Infusion of somatostatin along with insulin prevented the effects of diazoxide on plasma glucose and glucose production. It is concluded that diazoxide hyperglycemia is not due solely to decreased insulin secretion or increased epinephrine secretion and that glucagon is not a contributory factor. Diazoxide may act directly to increase glucose production and inhibit glucose uptake. Somatostatin appears capable of blocking the effect of diazoxide on glucose production by an unknown mechanism.
ISSN:0012-1797
1939-327X
DOI:10.2337/diab.26.10.931