Barrou Z, Seaquist E R, Robertson R P
Department of Medicine, University of Minnesota Medical School, Minneapolis.
Diabetes. 1994 May;43(5):661-6. doi: 10.2337/diab.43.5.661.
Although successful pancreas transplantation in humans with type I diabetes mellitus restores glucose-induced insulin secretion, provides freedom from insulin treatment, and normalizes fasting glucose levels, much less is known about its effects on counterregulation of hypoglycemia. To determine whether pancreas transplantation normalizes glucagon secretion and hepatic glucose production (HGP) during hypoglycemia, we performed hyperinsulinemic hypoglycemic clamps in successful recipients of pancreas allografts. Recipients were found to have glucagon secretory responses during hypoglycemia that were similar to those of control subjects (incremental glucagon response: recipients, 147 +/- 34 ng/L; control subjects, 161 +/- 43 ng/L, NS) but were significantly higher than those of matched subjects with type I diabetes (23 +/- 9 ng/L, P < 0.01). HGP rates at the end of 120 min of hypoglycemia were also significantly higher in recipients and control subjects than in subjects with diabetes (pancreas recipients, 1.92 +/- 0.33 mg.kg-1.min-1; control subjects, 2.05 +/- 0.18 mg.kg-1.min-1; subjects with type I diabetes, 0.58 +/- 0.12 mg.kg-1.min-1). A comparison with a third group of nondiabetic kidney transplant recipients demonstrated that the beneficial effects on glucose counterregulation were a result of pancreas transplantation and not the associated immunosuppressive therapy. We conclude that pancreas transplantation restores hypoglycemia-induced glucagon secretion and HGP, thereby allowing for normalization of glucose recovery from hypoglycemia.
虽然成功地对I型糖尿病患者进行胰腺移植可恢复葡萄糖诱导的胰岛素分泌，使患者无需接受胰岛素治疗，并使空腹血糖水平正常化，但对于其对低血糖反调节的影响却知之甚少。为了确定胰腺移植是否能使低血糖期间的胰高血糖素分泌和肝糖生成（HGP）正常化，我们对成功接受胰腺同种异体移植的患者进行了高胰岛素低血糖钳夹试验。结果发现，受者在低血糖期间的胰高血糖素分泌反应与对照受试者相似（胰高血糖素增量反应：受者为147±34 ng/L；对照受试者为161±43 ng/L，无显著性差异），但显著高于匹配的I型糖尿病受试者（23±9 ng/L，P<0.01）。低血糖120分钟结束时的HGP率在受者和对照受试者中也显著高于糖尿病受试者（胰腺移植受者为1.92±0.33 mg·kg-1·min-1；对照受试者为2.05±0.18 mg·kg-1·min-1；I型糖尿病受试者为0.58±0.12 mg·kg-1·min-1）。与第三组非糖尿病肾移植受者的比较表明，对葡萄糖反调节的有益作用是胰腺移植的结果，而非相关的免疫抑制治疗。我们得出结论，胰腺移植可恢复低血糖诱导的胰高血糖素分泌和HGP，从而使低血糖后的葡萄糖恢复正常化。
