Alternation in both insulin release and its hypoglycemic effects in atopic bronchial asthma.

In 31 patients with atopic bronchial asthma in clinical remission and in 21 healthy sex- and age-matched subjects, the responses to intravenous tolbutamide (1.0 gm) and insulin (0.1 U/kg) were studied over a period of 2 hr. In response to tolbutamide, asthmatics released significantly less insulin, but their blood glucose levels did not differ from those of controls. Asthmatics also reacted to tolbutamide-induced hypoglycemia with significantly greater output of growth hormone to blood. Following intravenous injection of insulin, the recovery of the blood glucose concentrations was significantly reduced in asthmatic patients. More economical use of insulin and increased responsiveness to its hypoglycemic action, together with the well-known reduction in hypoglycemic effects of catecholamines in bronchial asthma, might explain why asthmatics rarely develop diabetes mellitus.

The effects of prostacyclin on glycemia and insulin release in man.

Prostacyclin /PGI2/ administered intra-arterially or intravenously to patients with peripheral vascular disease exerted a hyperglycemic effect. In normoglycemic patients receiving PGI2 at a dose of 5 ng/kg/min these effects were barely detectable, but they became unmasked by a rapid glucose injection. In diabetic patients the same PGI1 dose led to distinct elevation in blood glucose. Prostacyclin at a dose of 10 ng/kg/min raised blood glucose levels both at rest and after stimulation with glucose, and opposed effectively hypoglycemic action of tolbutamide in non-diabetic patients. PGI2 repressed glucose-induced insulin release in some normoglycemic patients but in others it either increased it or did not affect it. While hyperglycemic effects are reversible when PGI2 infusion is stopped, and do not interfere with the usual therapeutic administration of prostacyclin for a few days they, nevertheless, might constitute a risk in a patient with poorly controlled diabetes.