ArticleDiabetes care2010
Clinical heterogeneity in monogenic diabetes caused by mutations in the glucokinase gene (GCK-MODY).
Article in Diabetes care, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 55 citations in OpenAlex.
- Trial
- Maturity Onset Diabetes of the Young (MODY): French National Diagnosis and Care Protocol (PNDS, Protocole National de Diagnostic et de Soins).Orphanet journal of rare diseases · 2026Review
- Case Report: New insights about clinical manifestations of patients withFrontiers in endocrinology · 2025Article
- Monogenic Defects of Beta Cell Function: From Clinical Suspicion to Genetic Diagnosis and Management of Rare Types of Diabetes.International journal of molecular sciences · 2024Review
- Tyrosol-loaded Nano-niosomes Attenuate Diabetic Injury by TargetingGlucose Metabolism, Inflammation, and Glucose Transfer.Pharmaceutical nanotechnology · 2024Article
- A comprehensive map of human glucokinase variant activity.Genome biology · 2023Article
- Sodium butyrate potentiates insulin secretion from rat islets at the expense of compromised expression of β cell identity genes.Cell death & disease · 2022Article
- Monogenic diabetes: a gateway to precision medicine in diabetes.The Journal of clinical investigation · 2021Review
- Phenotypic and Genetic Heterogeneity in a Thai Glucokinase MODY Family Reveals the Complexity of Young-Onset Diabetes.Frontiers in endocrinology · 2021Article
- Maturity-Onset Diabetes of the Young Identified Among Algerian Probands with Early-Onset Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- How Heterogeneity in Glucokinase and Gap-Junction Coupling Determines the Islet [CaBiophysical journal · 2019Article
- Not quite type 1 or type 2, what now? Review of monogenic, mitochondrial, and syndromic diabetes.Reviews in endocrine & metabolic disorders · 2018Review
- Phenotype Heterogeneity in Glucokinase-Maturity-Onset Diabetes of the Young (GCK-MODY) Patients.Journal of clinical research in pediatric endocrinology · 2017Article
- Comprehensive Maturity Onset Diabetes of the Young (MODY) Gene Screening in Pregnant Women with Diabetes in India.PloS one · 2017Article
- GCK gene mutations are a common cause of childhood-onset MODY (maturity-onset diabetes of the young) in Turkey.Clinical endocrinology · 2016Article
- Many faces of monogenic diabetes.Journal of diabetes investigation · 2014Review
- Repair of diverse diabetic defects of β-cells in man and mouse by pharmacological glucokinase activation.Diabetes, obesity & metabolism · 2012Review
- Serum levels of pancreatic stone protein (PSP)/reg1A as an indicator of beta-cell apoptosis suggest an increased apoptosis rate in hepatocyte nuclear factor 1 alpha (HNF1A-MODY) carriers from the third decade of life onward.BMC endocrine disorders · 2012Article
- Article
- Glucokinase links Krüppel-like factor 6 to the regulation of hepatic insulin sensitivity in nonalcoholic fatty liver disease.Hepatology (Baltimore, Md.) · 2012Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 5 countries.
Funding
Abstract
objectiveTo evaluate the heterogeneity in the clinical expression in a family with glucokinase mature-onset diabetes of the young (GCK-MODY). RESEARCH DESIGN AND
methodsMembers (three generations) of the same family presented either with overt neonatal hyperglycemia, marked postprandial hyperglycemia, or glucosuria. Homeostasis model assessment of insulin resistance (HOMA(IR)) and insulinogenic and disposition indexes were calculated. Oral glucose tolerance test (OGTT) results in the GCK mutation carriers from this family were compared with those from other subjects with GCK mutations in the same codon (GCK(261)), with other missense and other types of GCK mutations in different codons from the European MODY Consortium database (GCK(m)).
resultsMutation G261R was found in the GCK gene. During the OGTT, glucose (P = 0.02) and insulin (P = 0.009) response at 2 h as well as at the 2-h glucose increment (GCK(261) versus other missense GCK mutations, P = 0.003) were significantly higher in GCK(261) than in GCK(m) carriers.
conclusionsDiffering from other GCK(m) carriers, the glucose and insulin response to oral glucose was significantly higher in GCK(261) carriers, indicating clinical heterogeneity in GCK-MODY.
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