Incretin hormone responses to carbohydrate and protein/fat are preserved in adults with sulfonylurea-treated KCNJ11 neonatal diabetes

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  • Pamela Bowman
  • Kashyap A. Patel
  • Timothy J. McDonald
  • Holst, Jens Juul
  • Hartmann, Bolette
  • Maria Leveridge
  • Beverley M. Shields
  • Suzie Hammersley
  • Steve R. Spaull
  • Bridget A. Knight
  • Sarah E. Flanagan
  • Maggie H. Shepherd
  • Rob C. Andrews
  • Andrew T. Hattersley

The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are thought to be the main drivers of insulin secretion in individuals with sulfonylurea (SU)-treated KCNJ11 permanent neonatal diabetes. The aim of this study was to assess for the first time the incretin hormone response to carbohydrate and protein/fat in adults with sulfonylurea-treated KCNJ11 permanent neonatal diabetes compared with that of controls without diabetes. Participants were given a breakfast high in carbohydrate and an isocaloric breakfast high in protein/fat on two different mornings. Incremental area under the curve and total area under the curve (0-240 minutes) for total GLP-1 and GIP were compared between groups, using non-parametric statistical methods. Post-meal GLP-1 and GIP secretion were similar in cases and controls, suggesting this process is adenosine triphosphate-sensitive potassium channel-independent. Future research will investigate whether treatments targeting the incretin pathway are effective in individuals with KCNJ11 permanent neonatal diabetes who do not have good glycemic control on sulfonylurea alone.

TidsskriftJournal of Diabetes Investigation
Udgave nummer12
Sider (fra-til)1378-1382
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
This study was supported by the National Institute for Health and Care Research Exeter Biomedical Research Center, and National Institute for Health and Care Research Exeter Clinical Research Facility. The views expressed are those of the authors, and not necessarily those of the NIHR or the Department of Health and Social Care. The study also had grant support from a Sir George Alberti Clinical Research Training Fellowship funded by Diabetes UK (PB, grant number 16/0005407), a Wellcome Trust Senior Investigator Award (ATH, grant number 098395/Z/12/Z), a Wellcome Trust postdoctoral fellowship (KAP, grant number 110082/Z/15/Z), a Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society (SEF, grant number 105636/Z/14/Z). We thank Professor Fiona Gribble and Professor Frank Reimann (University of Cambridge) for their assistance with interpretation of the study data, and Professor Tamsin Ford (University of Cambridge) for academic supervisory support for PB during the study.

Publisher Copyright:
© 2023 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.

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