Glucoregulation during insulin and glucagon deficiency: role of catecholamines.
Glucose production decreases markedly following acute reduction in insulin and glucagon secretion (induced by somatostatin). After about an hour, however, glucose production is restored nearly to basal rates. To study the mechanism by which this occurs, islet hormone deficiency was superimposed on beta-adrenergic blockade. It was found that the hypoglycemia that accompanies insulin and glucagon deficiency is an adequate stimulus for catecholamine secretion. During combined hormone deficiency and beta-blockade, glucose production fell and remained very low for 2-3 h. This resulted in a profound hypoglycemia (glucose less than 30 mg/dl). We conclude from these studies that restoration of glucose production during sustained insulin and glucagon deficiency is not attributable to a) onset of insulin deficiency because insulin is equally depressed in both experimental settings, b) glucose autoregulation even though adequate substrate is available, or c) an alpha-adrenergic mechanism because plasma catecholamines were very high and alpha-receptors were not blocked. Rather, the glucose counterregulation during insulin and glucagon deficiency must be heavily dependent on a beta-adrenergic mechanism.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000409:Alanine / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D004837:Epinephrine / Q000097:blood; D005934:Glucagon / Q000172:deficiency*; D005943:Gluconeogenesis; D007328:Insulin / Q000172:deficiency*; D007700:Kinetics; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010215:Papio; D013004:Somatostatin
D000319:Adrenergic beta-Antagonists; D001786:Blood Glucose; D007328:Insulin; D013004:Somatostatin; D005934:Glucagon; D000409:Alanine; D009638:Norepinephrine; D004837:Epinephrine