Transient hepatic response to glucagon in @entity1 : role of @entity2690 and XXXX .

@entity1 @entity1009 @entity2690 @entity3190 @entity1943 @entity4854 @entity413
We infused glucagon into normal @entity1 while preventing changes in plasma @entity413 and @entity2690 . @entity2690 (0.45 mU . @entity1009 . kg-1) were infused for 90 min, while euglycemia was maintained by a variable @entity413 infusion. Subsequently, glucagon (6 ng . @entity1009 . kg-1) was added, and changes in plasma @entity413 were avoided by appropriately reducing the @entity413 infusion. With @entity2690 alone, @entity413 production (GP) fell to zero. When hyperglucagonemia (530 +/- 32 pg/ml) was superimposed, GP rose promptly and then slowly declined. However, between 180 and 240 min, GP remained elevated (1.72 +/- 0.30 mg . @entity1009 . kg-1) as compared to an @entity2690 control study (0.03 +/- 0.20, P less than 0.025). When @entity4854 (+25 mg/100 ml) was induced between 180 and 240 min, glucagon-stimulated GP was completely suppressed. To determine whether this effect was mediated by @entity4854 per se or @entity413 -induced @entity3190 , between 180 and 240 min we increased either a) the @entity2690 infusion (by 0.25 mU . @entity1009 . kg-1) while maintaining euglycemia or b) plasma @entity413 (+25 mg/100 ml) while blocking @entity2690 release with @entity1943 . When the @entity2690 was increased, GP declined by 68 +/- 13% (P less than 0.02). When plasma @entity413 alone was raised, GP fell from 1.44 +/- 0.09 to 0.07 +/- 0.16 mg . @entity1009 . kg-1 (less than 0.002). In conclusion, the hepatic response to sustained hyperglucagonemia is more persistent if changes in plasma @entity413 are prevented, and its transient nature is in part explained by a feedback adjustment to glucagon-induced @entity4854 and @entity3190 .
