Greco A V, Altomonte L, Ghirlanda G, D'Anna L M, Manna R, Caputo S, Uccioli L
Istituto di Clinica Medica, Università Cattolica del Sacro Cuore, Roma, Italy.
Acta Endocrinol (Copenh). 1988 Jul;118(3):337-45. doi: 10.1530/acta.0.1180337.
The present study was undertaken in order to establish the significance of glucagon in glucose intolerance in liver cirrhosis. The plasma glucose response to an oral glucose load (75 g) was determined in 10 control subjects and in 10 cirrhotic patients, after infusions of: glucagon (3 ng.kg-1.min-1) or saline (154 mmol/l); somatostatin (SRIH) (500 micrograms/h); and SRIH plus glucagon (3 ng.kg-1.min-1). Glucagon infusion did not impair glucose tolerance, neither in normal subjects nor in patients with cirrhosis. On the other hand, in both groups glucose tolerance was impaired by SRIH infusion, presumably owing to an absolute insulin deficiency. Both in normal subjects and in cirrhotic patients, SRIH plus glucagon infusion further impaired glucose tolerance, presumably as a result of excess glucagon and concomitant insulin deficiency. In conclusion, our data show that hyperglucagonemia is not an important factor in the development of the glucose intolerance in patients with hepatic cirrhosis.
本研究旨在确定胰高血糖素在肝硬化患者糖耐量异常中的意义。在10名对照受试者和10名肝硬化患者中，分别输注以下物质后，测定其对口服葡萄糖负荷（75克）的血糖反应：胰高血糖素（3纳克·千克⁻¹·分钟⁻¹）或生理盐水（154毫摩尔/升）；生长抑素（SRIH）（500微克/小时）；以及SRIH加胰高血糖素（3纳克·千克⁻¹·分钟⁻¹）。输注胰高血糖素并未损害正常受试者或肝硬化患者的糖耐量。另一方面，在两组中，输注SRIH均损害了糖耐量，推测是由于绝对胰岛素缺乏。在正常受试者和肝硬化患者中，输注SRIH加胰高血糖素均进一步损害了糖耐量，推测是由于胰高血糖素过量和伴随的胰岛素缺乏。总之，我们的数据表明，高胰高血糖素血症不是肝硬化患者糖耐量异常发生的重要因素。
