Cited by 90Pancreatic function and diabetesIon channel regulation and functionDiabetes and associated disorders

Successful transfer to sulfonylureas in KCNJ11 neonatal diabetes is determined by the mutation and duration of diabetes

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Babiker, Tarig, Vedovato, Natascia, Patel, Kashyap, Thomas, Nicholas, Finn, Roisin, Männikkö, Roope, Chakera, Ali J., Flanagan, Sarah E. +4 more·2016·Diabetologia

Abstract

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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Research works printed but not linked: 11

  1. [1]Flanagan SE Edghill EL Gloyn AL Mutations in KCNJ11, which encodes Kir6.2, are a common cause of diabetes diagnosed in the first 6 months of life, with the phenotype determined by genotype Diabetologia 2006 49 1190 1197 10.1007/s00125-006-0246-z 16609879 · DOI
  2. [2]Pearson ER Flechtner I Njølstad PR Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations N Engl J Med 2006 355 467 477 10.1056/NEJMoa061759 16885550 · DOI · Paper page
  3. [3]Shepherd M Transforming lives: transferring patients with neonatal diabetes from insulin to sulphonylureas Eur Diabetes Nurs 2006 3 137 142 10.1002/edn.60 · DOI
  4. [4]Thurber BW Carmody D Tadie EC Age at the time of sulfonylurea initiation influences treatment outcomes in KCNJ11-related neonatal diabetes Diabetologia 2015 58 1430 1435 10.1007/s00125-015-3593-9 25877689 PMC4641523 · DOI
  5. [5]McTaggart JS Clark RH Ashcroft FM The role of the KATP channel in glucose homeostasis in health and disease: more than meets the islet J Physiol 2010 588 3201 3209 10.1113/jphysiol.2010.191767 20519313 PMC2976015 · DOI
  6. [8]Gillis KD Gee WM Hammoud A Effects of sulfonamides on a metabolite-regulated ATPi-sensitive K+ channel in rat pancreatic B-cells Am J Physiol 1989 257 C1119 C1127 2514595
  7. [9]Shimomura K Flanagan SE Zadek B Adjacent mutations in the gating loop of Kir6.2 produce neonatal diabetes and hyperinsulinism EMBO Mol Med 2009 1 166 177 10.1002/emmm.200900018 20049716 PMC3378123 · DOI
  8. [11]Mlynarski W Tarasov AI Gach A Sulfonylurea improves CNS function in a case of intermediate DEND syndrome caused by a mutation in KCNJ11 Nat Clin Pract Neurol 2007 3 640 645 10.1038/ncpneuro0640 17982434 · DOI
  9. [12]Shimomura K Girard CAJ Proks P Mutations at the same residue (R50) of Kir6.2 (KCNJ11) that cause neonatal diabetes produce different functional effects Diabetes 2006 55 1705 1712 10.2337/db05-1640 16731833 · DOI
  10. [13]Girard CAJ Shimomura K Proks P Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes Pflugers Arch Eur J Physiol 2006 453 323 332 10.1007/s00424-006-0112-3 17021801 · DOI
  11. [14]O’Connell SM Proks P Kramer H The value of in vitro studies in a case of neonatal diabetes with a novel Kir6.2-W68G mutation Clin Case Rep 2015 3 884 887 10.1002/ccr3.370 26509030 PMC4614663 · DOI

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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.
Venue
Diabetologia
Published
2016-03-31
Volume
59
Issue
6
Pages
1162-1166
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
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
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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