# Glucometabolism in Kidney Transplant Recipients with and without Posttransplant Diabetes: Focus on Beta-Cell Function

## TL;DR

This study finds that beta-cell dysfunction is the main issue in posttransplant diabetes, more so than insulin resistance, in kidney transplant patients.

## Contribution

The study provides new evidence that beta-cell dysfunction is the primary defect in posttransplant diabetes.

## Key findings

- Model-based glucose sensitivity was more than 50% lower in PTDM patients compared to non-PTDM patients.
- Basic indices of beta-cell function were significantly reduced in patients with PTDM.
- Insulin sensitivity defects were present but less pronounced than beta-cell dysfunction in PTDM.

## Abstract

Posttransplant diabetes mellitus (PTDM) is a common complication after kidney transplantation. Pathophysiologically, whether beta-cell dysfunction rather than insulin resistance may be the predominant defect in PTDM has been a matter of debate. The aim of the present analysis was to compare glucometabolism in kidney transplant recipients with and without PTDM. To this aim, we included 191 patients from a randomized controlled trial who underwent oral glucose tolerance tests (OGTTs) 6 months after transplantation. We derived several basic indices of beta-cell function and insulin resistance as well as variables from mathematical modeling for a more robust beta-cell function assessment. Mean ± standard deviation of the insulin sensitivity parameter PREDIM was 3.65 ± 1.68 in PTDM versus 5.46 ± 2.57 in NON-PTDM. Model-based glucose sensitivity (indicator of beta-cell function) was 68.44 ± 57.82 pmol∙min−1∙m−2∙mM−1 in PTDM versus 143.73 ± 112.91 pmol∙min−1∙m−2∙mM−1 in NON-PTDM, respectively. Both basic indices and model-based parameters of beta-cell function were more than 50% lower in patients with PTDM, indicating severe beta-cell impairment. Nonetheless, some defects in insulin sensitivity were also present, although less marked. We conclude that in PTDM, the prominent defect appears to be beta-cell dysfunction. From a pathophysiological point of view, patients at high risk for developing PTDM may benefit from intensive treatment of hyperglycemia over the insulin secretion axis.