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Paradoxical Maturity-Onset Diabetes of the Young Arising From Loss-of-Function Mutations in ATP-Sensitive Potassium Channels.

Diabetes - 1 Jan 2026

Scala Rosa, Li Yunpeng, Gao Jian, York Nathan W, Unnikrishnan Ranjit, Anjana Ranjit Mohan, Mohan Viswanathan, Sundaramoorthy Gopi, Kavitha Babu, Radha Venkatesan, Nichols Colin G

Abstract excerpt

Pancreatic β-cell ATP-sensitive K+ (KATP) channel closure underlies electrical excitability and insulin release, but loss or inhibition of KATP channels can lead to paradoxical crossover from hyperinsulinism plus hypoglycemia, to glucose intolerance or diabetes. We report genotype-phenotype information from a set of patients clinically diagnosed with maturity-onset diabetes of the young (MODY) and carrying coding...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 40272924
DOI: 10.2337/db25-0110
PMCID: PMC12716611

Genes

ABCC8

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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