Defective glucagon secretion during sustained hypoglycemia following successful islet allo- and autotransplantation in humans
Abstract
Defective glucagon secretion during hypoglycemia is characteristic of long-standing type I diabetes. To determine whether this defect can be corrected by successful intrahepatic islet transplantation, we performed studies of hypoglycemia in four nondiabetic patients with chronic pancreatitis who had undergone total pancreatectomy and successful intrahepatic islet autotransplantation, in two type I diabetic recipients of successful intrahepatic islet allotransplantation, and in matched control subjects. We examined 1) whether intrahepatic islet autotransplantation provides glucagon secretion during prolonged periods of hypoglycemia and 2) whether intrahepatic islet allotransplantation in type I diabetic patients and consequent long-term normoglycemia reestablishes native alpha-cell responses to hypoglycemia. Glucagon secretion was assessed during 3-h hypoglycemic hyperinsulinemic clamp studies. The islet autograft recipients were studied 63 +/- 19 months posttransplant, and all were insulin-independent and normoglycemic (HbA(1c), 5.8 +/- 0.2%). Neither allograft recipient required exogenous insulin and maintained HbA(1c) levels of 5.7 and 6.4% 30 and 34 months posttransplant, respectively. All recipients were normoglycemic (fast...Continue Reading
Citations
Pancreatic islet transplantation for diabetes: successes, limitations, and challenges for the future
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