Almdal T P, Vilstrup H
Division of Hepatology, Rigshospitalet, Copenhagen, Denmark.
Endocrinology. 1988 Nov;123(5):2182-6. doi: 10.1210/endo-123-5-2182.
Rats weighing 220 g were injected sc with zinc protamin glucagon 20 micrograms once daily (recurrent hyperglucagonemia) and zinc protamin glucagon 60 micrograms 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 mumol/(min.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 less than 0.05 vs. control) and urea nitrogen synthesis rate 4.5 +/- 0.8 mumol/(min.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 less than 0.05 vs. control) and UNSR 7.9 +/- 0.8 mumol/(min.100g BW) (P less than 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 less than 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 less than 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.
给体重220克的大鼠皮下注射鱼精蛋白锌胰高血糖素，剂量为每日一次20微克（反复性高胰高血糖素血症）以及每日三次60微克（慢性高胰高血糖素血症）；对照组大鼠每日接受三次赋形剂注射。在第一组中，血中胰高血糖素每天有5小时升至200纳克/升以上；在第二组中，其持续保持在600纳克/升以上。在治疗2天（n = 5）和14天（n = 5）后，对照组大鼠全血α-氨基氮（AAN）浓度为4.3±0.1毫摩尔/升，尿素氮合成率为4.9±0.4微摩尔/（分钟·100克体重）（平均值±标准误）。在反复性高胰高血糖素血症大鼠中，治疗2天（n = 5）和14天（n = 5）后，总AAN为3.6±0.2毫摩尔/升（与对照组相比P < 0.05），尿素氮合成率为4.5±0.8微摩尔/（分钟·100克体重）。在慢性高胰高血糖素血症大鼠中，治疗2天（n = 5）和14天（n = 5）后，总AAN为2.2±0.1毫摩尔/升（与对照组相比P < 0.05），尿素氮合成率为7.9±0.8微摩尔/（分钟·100克体重）（与对照组相比P < 0.05）。对照组和反复性高胰高血糖素血症期间尿素排泄相同，但在慢性高胰高血糖素血症期间增加了50%。所有组的食物摄入量相同。慢性高胰高血糖素血症使氮平衡从10毫摩尔/24小时降至5毫摩尔/24小时（P < 0.05）。反复性高胰高血糖素血症未使器官总氮含量改变，但在慢性高胰高血糖素血症时， carcass、肠道、肝脏和肾脏中的总氮含量降至65 - 85%（P < 0.01）。总之，慢性而非反复性高胰高血糖素血症会增加尿素合成速率并降低血氨基酸浓度。这被认为是慢性高胰高血糖素血症导致器官氮流失的一个原因。
