Abstract
Abstract Administration of hydrazine to fasted rats results in a state of hypoglycemia which slowly abates over a period of several hours. Hydrazine also abolishes the increase in blood glucose normally seen after administration of hydrocortisone to fasted rats. Comparison of the concentrations of hepatic metabolites of rats treated with hydrazine with those of control rats reveals that hydrazine causes accumulations of lactate, pyruvate, citrate, malate, and oxalacetate coincident with less than normal amounts of phosphoenolpyruvate, 2- and 3-phosphoglyceric acids, and hexose monophosphates. The metabolic crossover point between oxalacetate and phosphoenolpyruvate is an indication that hydrazine in vivo inhibits the conversion of oxalacetate to phosphoenolpyruvate. Hydrazine in vitro inhibits rat liver phosphoenolpyruvate carboxykinase noncompetitively with respect to oxalacetate. Hydrazine also appears to inhibit renal gluconeogenesis. These data offer a possible explanation for the well-known hypoglycemic effect of hydrazine. Hydrocortisone is capable of increasing further the accumulations of malate and citrate in hydrazine-treated, fasted, adrenalectomized rats, whereas glucose depresses the accumulations of these same metabolites in normal rats treated with hydrazine. These observations are consistent with the known effects of hydrocortisone and glucose on gluconeogenesis and clearly demonstrate that these agents are capable of affecting reactions early in the over-all process of the synthesis of glucose.
Highlights
This paper reports data which suggest that hydrazine inhibits the conversion of oxalacetate to phosphoenolpyruvate, a conversion that is considered essential to the synthesis of glucose in hepatic and renal tissue
Effect of Hydra&e on Blood Glucose-Data presented in Fig. 1A show the blood glucose concentrations of 24-hour fasted, normal, male rats treated with 2 mmoles of NatSO or hydrazine per kg, body wt, at zero time and killed at intervals ranging from 4 to 5 hours after treatment
As little as 0.2 mmole causes a substantial decrease in blood glucose and the administration of 0.5, 1.0, and 2.0 mmoles causes a further decrease in blood glucose to approximately the same level at all three doses
Summary
Normal and adrenalectomized male albino rats, weighing 160 to 180 g, obtained from the Badger Research Corporation, Madison, Wisconsin, were used in all experiments. Adrenalectomized rats were used 7 days postoperatively. Water and 1yO NaCl solution were available at all times to normal and adrenalectomized rats, respectively. The procedures used for killing of the rats, removal of liver tissue, and the subsequent extraction of liver tissue, as well as the methods used in assaying the extracts for the various metabolites have previously been described [8, 9]. Similar procedures were used for the preparation of kidney extracts except that the animals were anesthetized with ether in order to facilitate the rapid removal of their kidneys. Blood samples for analyses of metabolites were taken from anesthetized rats by heart puncture
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