No influence of immunosuppression on insulin sensitivity and beta-cell function in living donor liver transplantation

Transplant Proc. 2005 May;37(4):1861-4. doi: 10.1016/j.transproceed.2005.02.093.

Abstract

In liver transplantation alterations of glucose metabolism are common but not well understood. Influence of immunosuppression is widely presumed but has not proven until now. Using a frequently sampled intravenous glucose tolerance test with a minimal modeling technique of glucose disappearance we analyzed insulin sensitivity (SI) and beta-cell function (first and second phase of pancreatic beta-cell secretion, Phi 1 and Phi 2) in living donor liver transplantation of the right lobe. Initial immunosuppression in recipients was done with tacrolimus, prednisolone, and basiliximab induction. Donors and recipients were investigated before and 10 days, 6 months, and 1 year after operation. Normal SI of controls (donors before operation) decreased markedly 10 days after right lobectomy to SI 2.22 +/- 0.35 x 10(-4) min(-1) x microU/mL (P < .001); Phi 2 was compensatory increased. All parameters normalized within 1 year. Recipients were insulin-resistant with hyperinsulinemia before transplantation. After transplantation no parameter was significantly different from donors; all normalized equally to donors over 1-year follow-up. Thus, immunosuppression in recipients has no influence on glucose metabolism because liver function itself seems to play a more pronounced role than known until now.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Blood Glucose / metabolism
  • Drug Therapy, Combination
  • Female
  • Glucose Tolerance Test
  • Humans
  • Immunosuppressive Agents / pharmacology*
  • Insulin / metabolism*
  • Insulin Secretion
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism*
  • Liver Diseases / classification
  • Liver Diseases / surgery
  • Liver Transplantation / physiology*
  • Living Donors*
  • Male
  • Middle Aged

Substances

  • Blood Glucose
  • Immunosuppressive Agents
  • Insulin