Successful transfer to sulfonylureas in KCNJ11 neonatal diabetes is determined by the mutation and duration of diabetes
Open accessAbstract
AIMS/HYPOTHESIS: The finding that patients with diabetes due to potassium channel mutations can transfer from insulin to sulfonylureas has revolutionised the management of patients with permanent neonatal diabetes. The extent to which the in vitro characteristics of the mutation can predict a successful transfer is not known. Our aim was to identify factors associated with successful transfer from insulin to sulfonylureas in patients with permanent neonatal diabetes due to mutations in KCNJ11 (which encodes the inwardly rectifying potassium channel Kir6.2). METHODS: We retrospectively analysed clinical data on 127 patients with neonatal diabetes due to KCNJ11 mutations who attempted to transfer to sulfonylureas. We considered transfer successful when patients completely discontinued insulin whilst on sulfonylureas. All unsuccessful transfers received ≥0.8 mg kg(-1) day(-1) glibenclamide (or the equivalent) for >4 weeks. The in vitro response of mutant Kir6.2/SUR1 channels to tolbutamide was assessed in Xenopus oocytes. For some specific mutations, not all individuals carrying the mutation were able to transfer successfully; we therefore investigated which clinical features could predict a successful transfer. RESULTS: In all, 112 out of 127 (88%) patients successfully transferred to sulfonylureas from insulin with an improvement in HbA1c from 8.2% (66 mmol/mol) on insulin, to 5.9% (41 mmol/mol) on sulphonylureas (p = 0.001). The in vitro response of the mutation to tolbutamide determined the likelihood of transfer: the extent of tolbutamide block was <63% for the p.C166Y, p.I296L, p.L164P or p.T293N mutations, and no patients with these mutations successfully transferred. However, most individuals with mutations for which tolbutamide block was >73% did transfer successfully. The few patients with these mutations who could not transfer had a longer duration of diabetes than those who transferred successfully (18.2 vs 3.4 years, p = 0.032). There was no difference in pre-transfer HbA1c (p = 0.87), weight-for-age z scores (SD score; p = 0.12) or sex (p = 0.17). CONCLUSIONS/INTERPRETATION: Transfer from insulin is successful for most KCNJ11 patients and is best predicted by the in vitro response of the specific mutation and the duration of diabetes. Knowledge of the specific mutation and of diabetes duration can help predict whether successful transfer to sulfonylureas is likely. This result supports the early genetic testing and early treatment of patients with neonatal diabetes aged under 6 months.
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Sulfonylurea drugs provide an effective therapy in >90% of patients with neonatal diabetes due to KATP mutations.
“Sulfonylurea drugs, which bypass metabolism and block the channel directly, provide an effective therapy in >90% of patients (44, 504).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [44]
The Introduction says sulfonylureas directly close KATP channels, and the Discussion reports that most patients with KCNJ11-related neonatal diabetes achieved near-normal glycaemia after switching. But the reported success rate is 88%, not >90%, and the study does not establish that rate for all KATP mutations. (LLM, conf=0.90)
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Cites
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Research works printed but not linked: 11
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Rorsman, P., & Ashcroft, F. M. (2018) · Physiological Reviews · doi:10.1152/physrev.00008.2017 · Cited by 793 · see citing works
Self-citationHattersley, A. T., Greeley, S. A. W., Polak, M., Rubio-Cabezas, O., Njølstad, P. R., Mlynarski, W., Castano, L., Carlsson, A., Raile, K., Chi, D. V., et al. (2018) · Pediatric Diabetes · doi:10.1111/pedi.12772 · Cited by 319 · see citing works
Self-citationNew insights into KATP channel gene mutations and neonatal diabetes mellitus
Pipatpolkai, T., Usher, S., Stansfeld, P. J., & Ashcroft, F. M. (2020) · Nature Reviews Endocrinology · doi:10.1038/s41574-020-0351-y · Cited by 122 · see citing works
Self-citationHyperglycaemia induces metabolic dysfunction and glycogen accumulation in pancreatic β-cells
Brereton, M. F., Rohm, M., Shimomura, K., Holland, C., Tornovsky-Babeay, S., Dadon, D., Iberl, M., Chibalina, M. V., Lee, S., Glaser, B., et al. (2016) · Nature Communications · doi:10.1038/ncomms13496 · Cited by 124 · see citing works
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- Authors
- Babiker, T., Vedovato, N., Patel, K., Thomas, N., Finn, R., Männikkö, R., Chakera, A. J., Flanagan, S. E., Shepherd, M. H., Ellard, S., Ashcroft, F. M., & Hattersley, A. T.
- Affiliations
- University of Exeter (GB)
- University of Oxford (GB)
- Corresponding author
- Ashcroft, Frances M.
- Hattersley, Andrew T.
- ORCID
- Venue
- Diabetologia
- Published
- 2016-03-31
- Volume
- 59
- Issue
- 6
- Pages
- 1162-1166
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- PMC
- PMC4869695
- OpenAlex
- W2313113438
- Cited by
- 90
- References
- 1
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 8 · 2023: 9 · 2022: 6 · 2021: 8 · 2020: 7 · 2019: 6 · 2018: 15 · 2017: 11 · 2016: 5
- FWCI
- 11.84
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Diabetologia (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Figshare (submittedVersion)
- Open Research Exeter (University of Exeter) (submittedVersion, cc-by)
- Royal Devon and Exeter Research Repository (Royal Devon and Exeter) (submittedVersion, cc-by)
- Funders
- Wellcome Trust
- National Institute for Health Research
- European Research Council
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- neonatal diabetes, KCNJ11 mutation, Kir6.2, sulfonylurea therapy, SUR1, glibenclamide, diabetes duration, potassium channel mutations, HbA1c, genotype-phenotype correlation, treatment response prediction
- MeSH terms
- Kcnj11 Channel, Blood Glucose, Diabetes Mellitus, Female, Humans, Hypoglycemic Agents, Infant, Infant, Newborn, Infant, Newborn, Diseases, Insulin, Male, Mutation, Retrospective Studies, Sulfonylurea Compounds, Multivariate Analysis, Potassium Channels, Inwardly Rectifying
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