Lee K U, Rhee B D, Lee H K, Kim C Y, Koh C S, Min H K
Diabetes Res Clin Pract. 1987 May-Jun;3(3):161-6. doi: 10.1016/s0168-8227(87)80022-0.
To elucidate the mechanism of glucose intolerance in chronic liver disease (CLD), the kinetics of plasma glucose, insulin and C-peptide were studied after intravenous glucose loading in patients with CLD. Fasting plasma insulin levels were higher in patients with CLD than in normal subjects. This hyperinsulinemia was attributed primarily to an increased pancreatic secretion of insulin. Patients with CLD were divided into two groups, one with normal fasting plasma glucose (FBS less than 100 mg/dl (Group I) and the other with higher FBS (Group II). In Group I, the glucose disappearance rate was normal and a brisk acute insulin response (AIR) to glucose was noted. The glucose disappearance rate in Group II was lower than that in normal subjects, and AIR to glucose was blunted. It is suggested that normal glucose tolerance in Group I patients could be interpreted as a state of compensation by hypersecretion of insulin. On the other hand, the glucose intolerance in Group II patients could be due to inadequate insulin secretion to overcome insulin resistance of CLD.
为阐明慢性肝病（CLD）中葡萄糖不耐受的机制，我们对CLD患者静脉注射葡萄糖负荷后血浆葡萄糖、胰岛素和C肽的动力学进行了研究。CLD患者的空腹血浆胰岛素水平高于正常受试者。这种高胰岛素血症主要归因于胰腺胰岛素分泌增加。CLD患者分为两组，一组空腹血糖正常（空腹血糖低于100mg/dl，第一组），另一组空腹血糖较高（第二组）。在第一组中，葡萄糖消失率正常，对葡萄糖有明显的急性胰岛素反应（AIR）。第二组的葡萄糖消失率低于正常受试者，对葡萄糖的AIR减弱。提示第一组患者的正常糖耐量可解释为胰岛素分泌过多的代偿状态。另一方面，第二组患者的葡萄糖不耐受可能是由于胰岛素分泌不足，无法克服CLD的胰岛素抵抗。
