AIM: The ability to generate a greater insulin response to an oral compared to an intravenous glucose load is the result of pancreatic stimulation by gut hormones and is known as the incretin effect (IE). A diminished IE is seen in diabetes and is associated with abnormal glucose tolerance (GT). We have recently reported that 30% of pancreas transplant subjects have abnormal glucose tolerance post-operatively, despite insulin independence and that this is associated with later graft failure. The incretin effect is thought to be mediated via a neuroendocrine axis and the role of the incretin effect in people receiving a denervated pancreas transplant is unknown. This study aimed to assess the incretin effect after pancreas transplantation

METHOD: The incretin effect was measured with extended frequently-sampled oral glucose tolerance tests and matched isoglycaemic intravenous glucose infusions in 10 pancreas transplant recipients and 10 kidney transplant recipients at 2 weeks and 3 months post-transplant, and in 10 healthy controls.

RESULTS: The groups were comparable for demographics. Isoglycaemia was achieved in each group. The pancreas transplant group at 2 weeks post-transplant showed lower glucose disposal compared to the kidney only transplant group and healthy controls (26.2% vs 42% vs 56.4%), with a significantly diminished incretin effect (7.5% vs 36.9% vs 46.5%, p<0.01) respectively. However, by 3 months, glucose disposal and the incretin effect had improved (26.2%-51.4% and 7.5%-27.4% respectively).

CONCLUSION: The present data suggest, for the first time, that pancreas transplantation may also be associated with a delay in establishing a full incretin effect. Whilst we cannot attribute a causal role, improvement at 3 months may represent re-innervation and future studies including an incretin therapy intervention trial are needed to determine whether incretin based therapies can improve long term pancreas transplant outcomes.

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