Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations
Open accessAbstract
BACKGROUND: Heterozygous activating mutations in KCNJ11, encoding the Kir6.2 subunit of the ATP-sensitive potassium (K(ATP)) channel, cause 30 to 58 percent of cases of diabetes diagnosed in patients under six months of age. Patients present with ketoacidosis or severe hyperglycemia and are treated with insulin. Diabetes results from impaired insulin secretion caused by a failure of the beta-cell K(ATP) channel to close in response to increased intracellular ATP. Sulfonylureas close the K(ATP) channel by an ATP-independent route. METHODS: We assessed glycemic control in 49 consecutive patients with Kir6.2 mutations who received appropriate doses of sulfonylureas and, in smaller subgroups, investigated the insulin secretory responses to intravenous and oral glucose, a mixed meal, and glucagon. The response of mutant K(ATP) channels to the sulfonylurea tolbutamide was assayed in xenopus oocytes. RESULTS: A total of 44 patients (90 percent) successfully discontinued insulin after receiving sulfonylureas. The extent of the tolbutamide blockade of K(ATP) channels in vitro reflected the response seen in patients. Glycated hemoglobin levels improved in all patients who switched to sulfonylurea therapy (from 8.1 percent before treatment to 6.4 percent after 12 weeks of treatment, P<0.001). Improved glycemic control was sustained at one year. Sulfonylurea treatment increased insulin secretion, which was more highly stimulated by oral glucose or a mixed meal than by intravenous glucose. Exogenous glucagon increased insulin secretion only in the presence of sulfonylureas. CONCLUSIONS: Sulfonylurea therapy is safe in the short term for patients with diabetes caused by KCNJ11 mutations and is probably more effective than insulin therapy. This pharmacogenetic response to sulfonylureas may result from the closing of mutant K(ATP) channels, thereby increasing insulin secretion in response to incretins and glucose metabolism. (ClinicalTrials.gov number, NCT00334711 [ClinicalTrials.gov].).
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Neonatal diabetes is most commonly due to activating mutations in genes encoding the ATP-sensitive potassium channel subunits Kir6.2 or SUR1.
“Findings that neonatal diabetes is most commonly due to activating mutations in genes encoding the ATP-sensitive potassium channel subunits Kir6.2 or SUR1”
From β-Cell Failure in Type 2 Diabetes: Postulated Mechanisms and Prospects for Prevention and Treatment (2014) · cites this paper as [6]
The paper's introductory text reports that activating Kir6.2 mutations account for 30–58% of permanent diabetes diagnosed before six months of age. The discussion says SUR1 mutations can also cause neonatal diabetes, but gives no frequency for them; it does not establish that the two mutations together are the most common cause of neonatal diabetes overall. Page numbers are not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredNeonatal diabetes due to Kir6.2 or SUR1 mutations can be treated with high-dose sulfonylureas despite being insulin dependent.
“can be treated with high-dose sulfonylureas despite being insulin dependent also provide a compelling case for genetic evaluation of monogenic diabetes with therapeutic and prognostic implications ( 2 – 6 ).”
From β-Cell Failure in Type 2 Diabetes: Postulated Mechanisms and Prospects for Prevention and Treatment (2014) · cites this paper as [6]
The Patients and Discussion sections (page not available) report that many insulin-treated patients with Kir6.2 mutations switched to sulfonylureas, including at relatively high doses. The paper also reports that four patients with SUR1 mutations switched from insulin to sulfonylureas, but it does not establish that they required or received high doses. (LLM, conf=0.87)
Experimental — accuracy not yet measuredSulfonylurea 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 [504]
The Abstract reports that 44 of 49 patients (90%) with Kir6.2 mutations successfully discontinued insulin after receiving sulfonylureas. It also says sulfonylureas close KATP channels by an ATP-independent route. The study therefore supports the mechanism and effectiveness for Kir6.2 mutations, but not the claim of effectiveness in >90% of patients with KATP mutations generally. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMore than 80% of people with diabetes diagnosed under 6 months of age have monogenic neonatal diabetes.
“As monogenic diabetes was less likely to have been considered in the past, molecular genetic testing for neonatal diabetes should be considered for all people with type 1 diabetes, regardless of current age, who were diagnosed under 6 months of age as more than 80% have monogenic neonatal diabetes, and the 30-50% with ATP-sensitive potassium (K ATP ) channel mutations can replace insulin with sulf”
From The management of type 1 diabetes in adults. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) (2021) · cites this paper as [33]
The introductory passage (page not provided) says KCNJ11 mutations account for 30–58% of permanent diabetes diagnosed before six months of age. The paper also recommends genetic testing for everyone diagnosed before six months, regardless of current age. Neither passage establishes the claimed figure that more than 80% have monogenic neonatal diabetes. (LLM, conf=0.82)
Experimental — accuracy not yet measured30-50% of people with ATP-sensitive potassium channel mutations can replace insulin with sulfonylureas.
“As monogenic diabetes was less likely to have been considered in the past, molecular genetic testing for neonatal diabetes should be considered for all people with type 1 diabetes, regardless of current age, who were diagnosed under 6 months of age as more than 80% have monogenic neonatal diabetes, and the 30-50% with ATP-sensitive potassium (K ATP ) channel mutations can replace insulin with sulf”
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- Authors
- Pearson, E. R., Flechtner, I., Njølstad, P. R., Malecki, M. T., Flanagan, S. E., Larkin, B., Ashcroft, F. M., Klimes, I., Codner, E., Iotova, V., Slingerland, A. S., Shield, J., Robert, J.-J., Holst, J. J., Clark, P. M., Ellard, S., Søvik, O., Polak, M., & Hattersley, A. T.
- Affiliations
- University of Dundee (GB)
- Hôpital Necker-Enfants Malades (FR)
- Haukeland University Hospital (NO)
- Jagiellonian University (PL)
- University of Exeter (GB)
- University of Oxford (GB)
- Medical University of Varna (BG)
- Leiden University Medical Center (NL)
- University of Copenhagen (DK)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2006-08-03
- Volume
- 355
- Issue
- 5
- Pages
- 467-477
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2164438031
- Cited by
- 988
- References
- 31
- Citations by year
- 2026: 21 · 2025: 21 · 2024: 26 · 2023: 37 · 2022: 33 · 2021: 49 · 2020: 44 · 2019: 45 · 2018: 65 · 2017: 56 · 2016: 65 · 2015: 59 · 2014: 64 · 2013: 64 · 2012: 47
- FWCI
- 61.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Discovery Research Portal (University of Dundee) (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Universidad de Chile (submittedVersion)
- Funders
- Sundhed og Sygdom, Det Frie Forskningsråd
- Wellcome Trust
- European Commission (LSHM-CT-2006-518153)
- Universitetet i Bergen
- Haukeland Universitetssjukehus
- Medical 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
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- KCNJ11, sulfonylureas, insulin therapy discontinuation, ATP-sensitive potassium channels, neonatal diabetes, glycemic control, insulin secretion, pharmacogenetics, HbA1c
- MeSH terms
- Kcnj11 Channel, Diabetes Mellitus, Female, Glyburide, Glycated Hemoglobin, Heterozygote, Humans, Hypoglycemic Agents, Infant, Infant, Newborn, Insulin, Male, Mutation, Receptors, Drug, Sulfonylurea Compounds, Tolbutamide, Potassium Channels, Cohort Studies, ATP-Binding Cassette Transporters, Potassium Channels, Inwardly Rectifying, Insulin-Secreting Cells, Sulfonylurea Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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