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Metabolism of Oral Glucose in Pancreas Transplant Recipients with Normal and Impaired Glucose Tolerance¹

Steno Diabetes Center (E.C.), Gentofte, Denmark; the Department of Transplantation Surgery, Huddinge Hospital (A.T.), Huddinge, Sweden; Novo Nordisk Research Institute (Aa.V., L.S.), Bagsvaerd, Denmark; and the Department of Medical Physiology, Panum Institute (J.J.H.), the Department of Nephrology, Rigshospitalet (K.R.), and the Department of Endocrinology, Hvidovre Hospital (S.M.), University of Copenhagen, Copenhagen, Denmark

Address all correspondence and requests for reprints to: Erik Christiansen, M.D., Steno Diabetes Center, Niels Steensensvej 2, 2820 Gentofte, Denmark.

To gain insight into the pathophysiology of impaired glucose tolerance in pancreas transplantation, glucose kinetics and insulin secretion were assessed after an oral glucose load in four combined pancreas-kidney recipients with impaired glucose tolerance (IPx), in five combined pancreas-kidney recipients with normal glucose tolerance, in six nondiabetic kidney transplant recipients, and in eight normal subjects employing a dual isotope technique. ß-Cell function was evaluated by calculating prehepatic insulin secretion rates, which subsequently were correlated to the ambient glucose concentrations to obtain an index of ß-cell responsiveness. Oxidative and nonoxidative glucose metabolism were assessed by indirect calorimetry. Basal insulin secretion rates, the glucose-stimulated early insulin secretion rates, as well as ß-cell responsiveness were markedly reduced in IPx than in the glucose-tolerant transplant subjects. Total systemic glucose appearance was similar in the groups with apparently comparable inhibition of systemic glucose release and increase in exogenous glucose appearance. The hyperglycemic response in IPx was due to a significant reduction in the glucose disappearance rates during the first 2 h after glucose ingestion. Nonoxidative glucose metabolism increased significantly less in IPx than in glucose-tolerant groups. Glucagon secretion was less suppressed in the early part of the study in IPx, which may have contributed to the excessive hyperglycemia.

In conclusion, IPx after pancreas transplantation was characterized by 1) impaired early insulin secretion, 2) reduced ß-cell responsiveness, 3) reduced glucose uptake, 4) impaired nonoxidative glucose metabolism, and 5) impaired early inhibition of glucagon secretion.

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