Mechanisms of postprandial hyperglycemia in liver transplant recipients: Comparison of liver transplant patients with kidney transplant patients and healthy controls

Impaired glucose tolerance or diabetes mellitus are frequent complications after organ transplantation, and are usually attributed to glucocorticoid a nd immunosuppressive treatments. Liver transplantation results in total hep atic denervation which may also affect glucoregulation. We therefore evalua ted postprandial glucose metabolism in a group of patients with liver cirrh osis before and after orthotopic liver transplantation. Seven patients with liver cirrhosis of various etiologies, 6 patients having received a kidney transplant, and 6 healthy subjects were studied. Their glucose metabolism was evaluated in the basal stare and over 4 hours after ingestion of a gluc ose load with 6.6 H-2 glucose dilution analysis. The patients with liver ci rrhosis were studied before, and again 4 weeks (range 2-6) and 38 weeks (ra nge 20-76, n = 6) after orthotopic liver transplantation. Basal glucose met abolism was similar in liver and kidney transplant recipients. Impaired glu cose tolerance was present in both groups, bur postprandial hyperglycemia w as exaggerated and lasted longer in liver transplant patients. Postprandial insulinemia was lower in liver transplant recipients, while C-peptide conc entrations were comparable to those of kidney transplant recipients, indica ting increased insulin clearance. Glucose turnover was not altered in both groups of patients during the initial 3 hours after glucose ingestion, but was higher in liver transplant early after transplantation during the fourt h hour. Postprandial hyperglycemia remained unchanged in liver transplant r ecipients 38 weeks after liver transplantation, despite substantial reducti on of immunosuppressive and glucocorticoid doses. We conclude that liver tr ansplant recipients have severe postprandial hyperglycemia which can be att ributed to insulinopenia (secondary, at least in part, to increased insulin clearance) and a late increased glucose turnover. These changes may be sec ondary to hepatic denervation.