Persistent effect of sustained hyperglucagonemia on glucose production in man.
In man prolonged infusions of glucagon cause a transient increase in glucose production. To determine whether this represents complete loss of effect of hyperglucagonemia on the liver or merely decreased hepatic responsiveness, glucagon (3 ng/kg/min) was infused in six normal subjects to produce sustained hyperglucagonemia for 180 min; at this time glucagon infusions were stopped for 60 min, then restarted at the same rate for 60 min and finally increased to 7.5 ng/kg/min for 30 min. Glucose production (Ra) and utilization (Rd) were measured isotopically. Initially glucagon infusion increased Ra transiently from 1.8 +/- 0.1 mg/kg/min to a maximum at 15 min of 2.5 +/- 0.2 mg/kg/min (p less than .01); Ra returned to basal values by 60 min and remained there until the glucagon infusion was stopped, whereupon it abruptly declined to a nadir of 1.4 +/- 0.1 mg/kg/min, a value significantly below baseline levels, p less than .005. Upon restarting the glucagon infusion, Ra increased to a similar extent as observed with the initial infusion and then returned to basal levels; when the glucagon infusion rate was increased to 7.5 ng/kg/min, Ra again increased. These results indicate that sustained hyperglucagonemia, despite apparent waning of its effect, continues to modulate hepatic glucose production.
D001786:Blood Glucose / Q000378:metabolism*; D005260:Female; D005934:Glucagon / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D007700:Kinetics; D008297:Male; D008657:Metabolic Clearance Rate
D001786:Blood Glucose; D007328:Insulin; D005934:Glucagon