Armando de Aguiar Pupo

Carbohydrate Metabolism in Hyperadrenocorticism

Investigations of tolerance to oral and intravenous glucose, intravenous and intra-arterial insulin, intravenous tolbutamide, and to subcutaneous glucagon were made in twelve patients with hyperadrenocorticism. The findings varied among patients, but certain trends were apparent. Fasting blood sugar concentrations tended to be low. The results of oral glucose tolerance teats were diabetic in eleven patients. The rate of glucose disappearance during glucose loading was normal or increased in all. Intravenous tolbutamide caused prolonged hypoglycemia in three of five patients. Hypoglycemia after intravenous and intra-arterial insulin was decreased. Depression of serum phosphorus was less than normal. Glucagon caused a rise in blood sugar above that of normals. The findings suggest that there is a normal or even increased rate of glucose utilization in clinical endogenous hyperadrenocorticism. The data are compatible with the view that the action of insulin on muscle tissue may be decreased with shift to other areas, perhaps adipose tissue.

Acute- and Late-Phase Insulin Secretion and Glucose Tolerance in Mild Alloxan Diabetes in Dogs

The acute and late phases of insulin secretion were studied in mongrel dogs before and after the induction of mild alloxan diabetes. Fasting glucose and insulin levels were unchanged from pretreatment values. The alloxan-diabetic dogs had significantly decreased early-phase insulin responses to glucose pulses (0.5 gm./kg.) and slower plasma glucose disappearance rates. In contrast, these mildly diabetic dogs achieved comparable insulin levels and higher glucose levels during a four-hour 40 mg./min. glucose infusion than pre-alloxan control values. Similar findings in human congenital mild diabetes have been interpreted as beta cell insensitivity or impedance to efficiency of plasma glucose uptake. The present observations in alloxan-induced mild diabetes in dogs suggest that reduced early-phase secretion and intact later phase of insulin secretion are not dependent on genetic determinants and may be induced in a model of acquired diabetes.

Treatment of Adrenocortical Cancer with O,P′-DDD

Excerpt The initial observations of Nelson and Woodward (1, 2) that the feeding of the insecticide, 1,1-dichloro-2,2-bis (p-chlorophenyl) ethane (DDD) to dogs results in necrosis and atrophy of the...

Influence of the vagus and splanchnic nerves on insulin secretion and glycemia

The role of the autonomic nervous system in control of the acute and the late-phase of insulin secretion was studied in mongrel dogs before and after bilateral severance of the vagus, splanchnic, and vagus plus splanchnic nerves. Glucose-stimulated acute insulin secretion increased after splanchnicotomy or transection of both autonomic nerves but remained unchanged after vagotomy alone. Late-phase insulin secretion was not altered by transection of any of the nerves alone or in combination; similar results were obtained as to fasting insulin levels. In contrast, fasting glycemia was increased after vagotomy and decreased after splanchnicotomy. These findings disclose tonic sympathetic and parasympathetic influences on blood glucose basal concentration and indicate an acute inhibitory role of the sympathetic system on insulin secretion.

ON THE MECHANISM OF INSULIN HYPERSENSITIVITY IN ADRENOCORTICAL INSUFFICIENCY.

A study of the sensitivity to a test dose of exogenous insulin was undertaken in eight patients with primary and five with secondary (Sheehans syndrome) adrenal insufficiency. The great majority showed hypersensitivity to insulin and hypoglycemia-unresponsiveness was present in all. The hypersensitivity was primarily the result of excessive peripheral insulin action as shown by the increased disappearance rate (k) of an intravenous glucose load, in the well nourished patient. A possible failure in glycogenesis and consequent reduced glucose release by the liver, which might explain the hypoglycemia-unresponsiveness, was not confirmed by the glucagon test, suggesting that if there is liver impairment it is in its rate of glucose release independent of the amount of glycogen present and related to the glucocorticoid influence on the threshold of blood glucose regulation by the liver.

PREDISPOSITION TO DIABETES AS EVALUATED BY THE CORTISONE-GLUCOSE TOLERANCE TEST IN CHILDREN; A PRELIMINARY STUDY.

Cortisone-glucose tolerance tests with progressively increasing doses of the steroid were performed in healthy children born to diabetic parents belonging to different mating types. The results suggest that predisposition to diabetes can be detected in younger offspring by using a critical dose of cortisone.