ArticleDiabetes2013
Metabolite profiling reveals normal metabolic control in carriers of mutations in the glucokinase gene (MODY2).
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.
- Insights from basic adjunctive examinations of GCK-MODY, HNF1A-MODY, and type 2 diabetes: A systemic review and meta-analysis.Journal of diabetes · 2023Pooled it
- Therapeutic effect and safety of curcumin in women with PCOS: A systematic review and meta-analysis.Frontiers in endocrinology · 2022Pooled it
- Underestimated risk of secondary complications in pathogenic and glucose-elevating GCK variant carriers with type 2 diabetes.Communications medicine · 2024Article
- Quantitative profiling and diagnostic potential of one-carbon and central metabolism pools in MODY2 and T1DM.Diabetology & metabolic syndrome · 2023Article
- Glucokinase Inactivation Ameliorates Lipid Accumulation and Exerts Favorable Effects on Lipid Metabolism in Hepatocytes.International journal of molecular sciences · 2023Article
- Identification and management of GCK-MODY complicating pregnancy in Chinese patients with gestational diabetes.Molecular and cellular biochemistry · 2022Article
- Elevated level of lysophosphatidic acid among patients with HNF1B mutations and its role in RCAD syndrome: a multiomic study.Metabolomics : Official journal of the Metabolomic Society · 2022Article
- Liver nucleotide biosynthesis is linked to protection from vascular complications in individuals with long-term type 1 diabetes.Scientific reports · 2020Article
- Using Clinical Indices to Distinguish MODY2 (GCK Mutation) and MODY3 (HNF1A Mutation) from Type 1 Diabetes in a Young Chinese Population.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2019Article
- Birthweight correlates with later metabolic abnormalities in Chinese patients with maturity-onset diabetes of the young type 2.Endocrine · 2019Article
- A new clinical screening strategy and prevalence estimation for glucokinase variant-induced diabetes in an adult Chinese population.Genetics in medicine : official journal of the American College of Medical Genetics · 2019Article
- Dysregulation of Glucagon Secretion by Hyperglycemia-Induced Sodium-Dependent Reduction of ATP Production.Cell metabolism · 2019Article
- Monogenic Diabetes in Children and Adolescents: Recognition and Treatment Options.Current diabetes reports · 2018Review
- Phenotype Heterogeneity in Glucokinase-Maturity-Onset Diabetes of the Young (GCK-MODY) Patients.Journal of clinical research in pediatric endocrinology · 2017Article
- The impact of Roux-en-Y gastric bypass surgery on normal metabolism in a porcine model.PloS one · 2017Article
- Undiagnosed MODY: Time for Action.Current diabetes reports · 2015Review
- Deletion of glycerol channel aquaporin-9 (Aqp9) impairs long-term blood glucose control in C57BL/6 leptin receptor-deficient (db/db) obese mice.Physiological reports · 2015Article
- Less but better: cardioprotective lipid profile of patients with GCK-MODY despite lower HDL cholesterol level.Acta diabetologica · 2014Article
- Clinical and non-targeted metabolomic profiling of homozygous carriers of Transcription Factor 7-like 2 variant rs7903146.Scientific reports · 2014Article
- Improved Glucose-Stimulated Insulin Secretion by Selective Intraislet Inhibition of Angiotensin II Type 1 Receptor Expression in Isolated Islets of db/db Mice.International journal of endocrinology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the gene encoding glucokinase (GCK) cause a mild hereditary form of diabetes termed maturity-onset diabetes of the young (MODY)2 or GCK-MODY. The disease does not progress over time, and diabetes complications rarely develop. It has therefore been suggested that GCK-MODY represents a metabolically compensated condition, but experimental support for this notion is lacking. Here, we profiled metabolites in serum from patients with MODY1 (HNF4A), MODY2 (GCK), MODY3 (HNF1A), and type 2 diabetes and from healthy individuals to characterize metabolic perturbations caused by specific mutations. Analysis of four GCK-MODY patients revealed a metabolite pattern similar to that of healthy individuals, while other forms of diabetes differed markedly in their metabolite profiles. Furthermore, despite elevated glucose concentrations, carriers of GCK mutations showed lower levels of free fatty acids and triglycerides than healthy control subjects. The metabolite profiling was confirmed by enzymatic assays and replicated in a cohort of 11 GCK-MODY patients. Elevated levels of fatty acids are known to associate with β-cell dysfunction, insulin resistance, and increased incidence of late complications. Our results show that GCK-MODY represents a metabolically normal condition, which may contribute to the lack of late complications and the nonprogressive nature of the disease.
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