Loss of Nitrogen from Organs in Rats Induced by Exogenous Glucagon*

Abstract

Rats weight 220 g were injected sc with zinc protamin glucagon 20 .mu.g once daily (recurrent hyperglucagonemia) and zinc protamin glucagon 60 .mu.g three times daily (chronic hyperglucagonemia); the controls received the vehicle three times daily. In the first group blood glucagon rose to above 200 ng/liter for 5 h every day; in the second group it constantly stayed above 600 ng/liter. After both 2 (n = 5) and 14 (n = 5) days treatment the control total blood .alpha.-amino-nitrogen (AAN) concentration was 4.3 .+-. 0.1 mmol/liter, and the urea nitrogen synthesis rate was 4.9 .+-. 0.4 .mu.mol/(min .cntdot. 100 g BW) (mean .+-. SEM) in controls. In recurrent hyperglucagonemic rats, treated for both 2 (n = 5) and 14 (n = 5) days, total AAN was 3.6 .+-. 0.2 mmol/liter (P < 0.05 vs. control) and urea nitrogen synthesis rate 4.5 .+-. 0.8 .mu.mol/(min .cntdot. 100 g BW). In chronic hyperglucagonemic, treated for both 2 (n = 5) and 14 (n = 5) days, total AAN was 2.2 .+-. 0.1 mmol/liter (P < 0.05 vs. control) and UNSR 7.9 .+-. 0.8 .mu.mol/(min .cntdot. 100 g BW) (P < 0.05 vs. control). The urea excretion was identical in controls and during recurrent hyperglucagonemia, but it was increased by 50% during chronic hyperglucagonemia. Food intake was the same in all groups. N Balances decreased from 10 mmol/24 h to 5 mmol/24 h (P < 0.05) by chronic hyperglucagonemia. The total organ N content did not change by recurrent hyperglucagonemia, but in chronic hyperglucagonemia it decreased to 65-85% (P < 0.01) in carcass, intestines, liver, and kidneys. In conclusion chronic but not recurrent hyperglucagonemia increases the rate of urea synthesis and decreases the blood amino acid concentration. This is suggested to be a reason for the loss of N from organs by chronic hyperglucagonemia.