Beta‐cell death and dysfunction drives hyperglycaemia in organ donors
Authors' conclusion
In pancreas donors, hyperglycaemia requiring IT is strongly associated with beta-cell death. This provides an explanation for the relationship of donor IT with post-transplant beta-cell dysfunction in transplant recipients.
Study context
- Population
- Pancreas donors after brain death40 (43%) required insulin
- Participants
- 92 donors
- Exposure
- Insulin-treated vs not insulin-treated donors
- ITn = 40
- Outcome
- Relationships between donor insulin use and markers of beta-cell death (INS-cfDNA, miR-375) and beta-cell function
Main finding
As reported in the abstract
- Peak glucose, median (IQR): IT 8 (7-11) vs not-IT 6 (6-8) mmol/L; p = .016
- C-peptide, median (IQR): IT 3280 (3159-3386) vs not-IT 3195 (2868-3386) pmol/L; p = .046
- INS-cfDNA, median (IQR): IT 35 (18-52) vs not-IT 30 (8-51) copies/ml; p = .035
- miR-375, median (IQR): IT 1.050 (0.19-1.95) vs not-IT 0.73 (0.32-1.10) copies/nl; p = .05
Observational data: associations, not effects.
Further findings
Donor miR-375 predicting recipient islet graft failure · 3 months
- Adjusted ROC (SE)
- 0.813 (0.149)
Original publication
Beta‐cell death and dysfunction drives hyperglycaemia in organ donors. Diabetes Obes Metab. Published 30 August 2023. doi:10.
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