Glucometabolism in kidney transplant recipients with and without posttransplant diabetes: Focus on beta-cell function
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- dc.contributor.author Kurnikowski, Amelie
- dc.contributor.author Salvatori, Benedetta
- dc.contributor.author Krebs, Michael
- dc.contributor.author Budde, Klemens
- dc.contributor.author Eller, Kathrin
- dc.contributor.author Pascual Santos, Julio
- dc.contributor.author Morettini, Micaela
- dc.contributor.author Göbl, Christian
- dc.contributor.author Hecking, Manfred
- dc.contributor.author Tura, Andrea
- dc.date.accessioned 2024-10-01T06:32:35Z
- dc.date.available 2024-10-01T06:32:35Z
- dc.date.issued 2024
- dc.description.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.
- dc.format.mimetype application/pdf
- dc.identifier.citation Kurnikowski A, Salvatori B, Krebs M, Budde K, Eller K, Pascual J, et al. Glucometabolism in kidney transplant recipients with and without posttransplant diabetes: Focus on beta-cell function. Biomedicines. 2024 Jan 30;12(2):317. DOI: 10.3390/biomedicines12020317
- dc.identifier.doi http://dx.doi.org/10.3390/biomedicines12020317
- dc.identifier.issn 2227-9059
- dc.identifier.uri http://hdl.handle.net/10230/61280
- dc.language.iso eng
- dc.publisher MDPI
- dc.relation.ispartof Biomedicines. 2024 Jan 30;12(2):317
- dc.rights © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
- dc.rights.accessRights info:eu-repo/semantics/openAccess
- dc.rights.uri http://creativecommons.org/licenses/by/4.0/
- dc.subject.keyword NODAT
- dc.subject.keyword PTDM
- dc.subject.keyword Beta-cell function
- dc.subject.keyword Endocrine pancreas
- dc.subject.keyword Insulin resistance
- dc.subject.keyword Kidney transplantation
- dc.subject.keyword Pancreatic alpha-cell
- dc.title Glucometabolism in kidney transplant recipients with and without posttransplant diabetes: Focus on beta-cell function
- dc.type info:eu-repo/semantics/article
- dc.type.version info:eu-repo/semantics/publishedVersion