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Article

ATP-sensitive K+ channel signaling in glucokinase-deficient diabetes.

Diabetes - 1 Oct 2005

Remedi Maria S, Koster Joseph C, Patton Brian L, Nichols Colin G

Abstract excerpt

As the rate-limiting controller of glucose metabolism, glucokinase represents the primary beta-cell "glucose sensor." Inactivation of both glucokinase (GK) alleles results in permanent neonatal diabetes; inactivation of a single allele causes maturity-onset diabetes of the young type 2 (MODY-2). Similarly, mice lacking both alleles (GK(-/-)) exhibit severe neonatal diabetes and die within a week, whereas...

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Identifiers

PMID: 16186394
DOI: 10.2337/diabetes.54.10.2925

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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ATP-sensitive K+ channel signaling in glucokinase-deficient diabetes.PMID 16186394Read ↗

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Diverse roles of K(ATP) channels learned from Kir6.2 genetically engineered mice.Semantic proximity Read ↗

Cell-specific roles of glucokinase in glucose homeostasis.Semantic proximity Read ↗

Diabetes and insulin secretion: the ATP-sensitive K+ channel (K ATP) connection.Semantic proximity Read ↗

Glucose modulation of ATP-sensitive K-currents in wild-type, homozygous and heterozygous glucokinase knock-out mice.Semantic proximity Read ↗

Of mice and men: K(ATP) channels and insulin secretion.Semantic proximity Read ↗

Sex-dependent additive effects of dorzagliatin and incretin on insulin secretion in a novel mouse model of <i>GCK</i> -MODYSemantic proximity Read ↗

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Mutations in pancreatic ß-cell Glucokinase as a cause of hyperinsulinaemic hypoglycaemia and neonatal diabetes mellitus.Semantic proximity Read ↗

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