Evanescent effects of hypo- and hyperglucagonemia on blood glucose homeostasis.
Hypoglucagonemia (induced by somatostatin) and hyperglucagonemia (induced by infusion of physiologic amounts of glucagon) have only evanescent effects on blood glucose regulation. Despite on-going glucagon suppression by somatostatin, fasting hyperglycemia develops within 4-6 hr of insulin suppression, indicating that (1) basal glucagon secretion is not essential for the development of the diabetic state; and (2) insulin-deficiency (rather than altered glucagon secretion) is the dominant long-term factor determining glucose homeostasis in the diabetic. With respect to hyperglucagonemia, only a transient increase in splanchnic glucose output is observed in normal and diabetic subjects in response to physiologic increments in this hormone. The exaggerated hyperglycemic effect of glucagon observed in diabetics1 is thus a consequence of the failure to metabolize the glucose traniently released into the systemic circulation in response to the glucagon rather than a result of persistent stimulation of hepatic glucose production. These observations thus further underscore the essentiality of insulin deficiency in the diabetogenic action of glucagon.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D004285:Dogs; D005934:Glucagon / Q000097:blood*; D006503:Hepatic Veins; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000097:blood* / Q000494:pharmacology; D013004:Somatostatin / Q000494:pharmacology*
D001786:Blood Glucose; D007328:Insulin; D013004:Somatostatin; D005934:Glucagon