Hyperglucagonemia during insulin deficiency accelerates protein catabolism.
Hyperglucagonemia during insulin deficiency accelerates protein catabolism.
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胰岛素缺乏期间的高胰高血糖素血症会加速蛋白质分解代谢。
DOI：
10.1152/ajpendo.1987.253.2.e208
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Welle,SL
中科院分区：
文献类型：
--
作者：
Nair,KS;Halliday,D;Matthews,DE;Welle,SL
高胰高血糖素血症在尿氮排泄增加的许多情况下与胰岛素缺乏或胰岛素抵抗共存，但胰高血糖素在这些情况下的确切作用是有争议的。本研究的目的是评估高胰高血糖素血症对胰岛素缺乏受试者蛋白质代谢的影响。我们使用一种必需氨基酸（L-[1- 13 C]亮氨酸）的稳定同位素作为体内蛋白质代谢的示踪剂。通过静脉输注生长抑素诱导胰岛素和胰高血糖素联合缺乏。通过输注生长抑素和胰高血糖素诱导高胰高血糖素血症和低胰岛素血症。当单独输注生长抑素时，亮氨酸通量增加，表明蛋白水解增加6-17%。当输注生长抑素和胰高血糖素时，亮氨酸通量增加，表明蛋白水解增加12-32%。在输注生长抑素和胰高血糖素期间亮氨酸通量的增加高于单独输注生长抑素期间的增加。单独的生长抑素没有改变亮氨酸氧化，而生长抑素加胰高血糖素增加亮氨酸氧化100%。我们的结论是，高胰高血糖素血症加速蛋白水解和亮氨酸氧化在胰岛素缺乏的人。
Hyperglucagonemia coexists with insulin deficiency or insulin resistance in many conditions where urinary nitrogen excretion is increased, but the precise role of glucagon in these conditions is controversial. The purpose of this study was to evaluate the effect of hyperglucagonemia on protein metabolism in insulin-deficient subjects. We used the stable isotope of an essential amino acid (L-[1-13C]leucine) as a tracer of in vivo protein metabolism. A combined deficiency of insulin and glucagon was induced by intravenous infusion of somatostatin. Hyperglucagonemia and hypoinsulinemia were induced by infusions of somatostatin and glucagon. When somatostatin alone was infused leucine flux increased, indicating a 6-17% increase in proteolysis. When somatostatin and glucagon were infused, leucine flux increased, indicating a 12-32% increase in proteolysis. The increase in leucine flux during the infusion of somatostatin and glucagon was higher than the increase during infusion of somatostatin alone. Somatostatin alone did not change leucine oxidation, whereas the somatostatin plus glucagon increased leucine oxidation 100%. We conclude that hyperglucagonemia accelerates proteolysis and leucine oxidation in insulin-deficient humans.