Johnson D G, Alberti K G, Faber O K, Binder C
Lancet. 1977 Jan 1;1(8001):10-3. doi: 10.1016/s0140-6736(77)91652-x.
The breakdown of proinsulin in the pancreatic beta cell yields insulin and C-peptide which are secreted in equimolar amounts. Unlike insulin, C-peptide is not degraded significantly by the liver, so that its measurement should give a better assessment of insulin secretion than estimation of peripheral insulin levels alone; particularly in the presence of hepatic dysfunction. Plasma C-peptide and insulin response to an oral glucose load have therefore been assessed in 14 cirrhotic and 7 normal subjects. Cirrhotic patients were divided into hyperinsulinaemic and normoinsulinaemic groups based on fasting plasma-insulin concentrations. Fasting blood-blucose and plasma-C-peptide concentrations were the same in normal and cirrhotic subjects, suggesting that basal pancreatic insulin secretion was the same in all subjects. Thus the C-peptide/insulin ratio was significantly decreased in hyperinsulinaemic subjects (2-13 +/- 0-31, compared with 4-63 +/- 0-48 in controls). After oral glucose, the two groups of cirrhotic patients showed the same glucose intolerance. C-peptide concentrations were also the same but insulin concentrations were markedly increased in the hyperinsulinaemic group. It is suggested that pancreatic insulin secretion is not increased in cirrhosis and that the peripheral hyperinsulinism is due solely to decreased hepatic insulin degradation secondary to either spontaneous portal-systemic shunting or to parenchymal damage.
胰岛β细胞中胰岛素原的分解产生胰岛素和C肽，二者以等摩尔量分泌。与胰岛素不同，C肽在肝脏中不会被显著降解，因此，相较于仅评估外周胰岛素水平，检测C肽应能更好地评估胰岛素分泌情况；在存在肝功能障碍时尤其如此。因此，对14名肝硬化患者和7名正常受试者进行了口服葡萄糖负荷后血浆C肽和胰岛素反应的评估。根据空腹血浆胰岛素浓度，将肝硬化患者分为高胰岛素血症组和正常胰岛素血症组。正常受试者和肝硬化受试者的空腹血糖和血浆C肽浓度相同，这表明所有受试者的基础胰腺胰岛素分泌相同。因此，高胰岛素血症受试者的C肽/胰岛素比值显著降低（2.13±0.31，而对照组为4.63±0.48）。口服葡萄糖后，两组肝硬化患者的葡萄糖耐量相同。C肽浓度也相同，但高胰岛素血症组的胰岛素浓度显著升高。提示肝硬化时胰腺胰岛素分泌并未增加，外周高胰岛素血症完全是由于自发性门体分流或实质损伤继发的肝脏胰岛素降解减少所致。
