1944
DOI: 10.1038/154487a0
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Experimental Hyperglycæmia by Injection of Intermediary Fat Metabolism Products in Rabbits

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1946
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Cited by 21 publications
(6 citation statements)
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“…glycemia with decreased insulin in the blood and pancreas by day 70. These authors suggested that ketone bodies first stimulate insulin secretion with gradual exhaustion of islet cells supervening (29)(30)(31)(32)(33). Tidwell and Axelrod (34) also suggested that acetoacetate stimulates insulin release in the rat.…”
Section: Methodsmentioning
confidence: 99%
“…glycemia with decreased insulin in the blood and pancreas by day 70. These authors suggested that ketone bodies first stimulate insulin secretion with gradual exhaustion of islet cells supervening (29)(30)(31)(32)(33). Tidwell and Axelrod (34) also suggested that acetoacetate stimulates insulin release in the rat.…”
Section: Methodsmentioning
confidence: 99%
“…(143 ) depressed carbohydrate metabolism in men as judged from the blood sugar curves after glucose inj ection. Repeated injections of acetoacetate, �-hydroxybutyrate and pyruvate caused hyperglycemia in rabbits (144). Sokal (145) found that some liver extract prepara tions which are used therapeutically in the treatment of pernicious anemia contained a substance which caused hyperglycemia and glyco suria in men and rats.…”
Section: Experiments On Intact Animals and Changes In Blood Constituentsmentioning
confidence: 98%
“…Only scant attention, however, has been paid to the effects that hyperketonemia, in turn, might have on carbohydrate and fat metabolism. The conflicting results from such studies (13)(14)(15)(16)(17) have been reviewed recently (18). Studies in this laboratory, designed to define the effects of induced hyperketonemia on carbohydrate and fat metabolism (18,19), showed that iv infusions of ,8-hydroxybutyric acid, acetoacetic acid, or their sodium salts produced the following immediate changes in glucose and nonesterified fatty acid (NEFA) metabolism: 1) blood glucose concentration fell promptly, at times to distinctly hypoglycemic levels, 2) hepatic glucose output decreased sharply to less than 50% of control values, a reduction accounting entirely for the decrease in arterial glucose concentration, and 3) these changes in glucose metabolism were accompanied simultaneously by a greater than 50% fall in arterial plasma NEFA concentration.…”
mentioning
confidence: 99%