Antoniello S, La Rocca S, Cavalcanti E, Auletta M, Salvatore F, Cacciatore L
Cattedra di Medicina Interna, Università di Napoli, Naples, Italy.
Clin Chim Acta. 1989 Aug 31;183(3):343-50. doi: 10.1016/0009-8981(89)90369-0.
Hyperinsulinemia and impaired glucose tolerance are associated with liver cirrhosis. To investigate whether insulin-degrading activity in liver tissue plays a role in hyperinsulinemia, we assayed this activity in biopsy tissue from healthy and cirrhotic subjects. There was no difference in insulin degradation between these two groups. Also glucagon-degrading activity in liver tissue, which is catalyzed by the same enzyme as insulin-degrading activity, did not differ between the two groups studied. Therefore, insulin-degrading activity does not appear to be involved in the hyperinsulinemia that occurs in liver cirrhosis. The study provides indirect evidence that hyperinsulinemia and impaired glucose metabolism in liver cirrhosis are due to different mechanisms (receptorial and post-receptorial defects, and altered feedback inhibition of insulin secretion).
高胰岛素血症和糖耐量受损与肝硬化有关。为了研究肝组织中的胰岛素降解活性是否在高胰岛素血症中起作用，我们检测了健康受试者和肝硬化受试者活检组织中的这种活性。两组之间的胰岛素降解没有差异。同样，肝组织中由与胰岛素降解活性相同的酶催化的胰高血糖素降解活性在两组研究对象之间也没有差异。因此，胰岛素降解活性似乎与肝硬化中发生的高胰岛素血症无关。该研究提供了间接证据，表明肝硬化中的高胰岛素血症和糖代谢受损是由不同机制（受体和受体后缺陷，以及胰岛素分泌反馈抑制改变）所致。
