ArticleScientific reports2016
A suppressor locus for MODY3-diabetes.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Review
- Incomplete penetrance and variable expressivity in monogenic diabetes; a challenge but also an opportunity.Reviews in endocrine & metabolic disorders · 2023Review
- Obesogenic and diabetic effects of CD44 in mice are sexually dimorphic and dependent on genetic background.Biology of sex differences · 2022Article
- HNF1A Mutations and Beta Cell Dysfunction in Diabetes.International journal of molecular sciences · 2022Review
- Quantitative Proteomic Study Unmasks Fibrinogen Pathway in Polycystic Liver Disease.Biomedicines · 2022Article
- Human Pluripotent Stem Cells Go Diabetic: A Glimpse on Monogenic Variants.Frontiers in endocrinology · 2021Review
- Genome Editing Human Pluripotent Stem Cells to Model β-Cell Disease and Unmask Novel Genetic Modifiers.Frontiers in endocrinology · 2021Review
- HNF1α controls glucagon secretion in pancreatic α-cells through modulation of SGLT1.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Human stem cell models: lessons for pancreatic development and disease.Genes & development · 2019Review
- Modeling Monogenic Diabetes using Human ESCs Reveals Developmental and Metabolic Deficiencies Caused by Mutations in HNF1A.Cell stem cell · 2019Article
- HNF1Journal of diabetes research · 2019Article
- How mice are indispensable for understanding obesity and diabetes genetics.Current opinion in endocrinology, diabetes, and obesity · 2017Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maturity Onset Diabetes of the Young type 3 (MODY3), linked to mutations in the transcription factor HNF1A, is the most prevalent form of monogenic diabetes mellitus. HNF1alpha-deficiency leads to defective insulin secretion via a molecular mechanism that is still not completely understood. Moreover, in MODY3 patients the severity of insulin secretion can be extremely variable even in the same kindred, indicating that modifier genes may control the onset of the disease. With the use of a mouse model for HNF1alpha-deficiency, we show here that specific genetic backgrounds (C3H and CBA) carry a powerful genetic suppressor of diabetes. A genome scan analysis led to the identification of a major suppressor locus on chromosome 3 (Moda1). Moda1 locus contains 11 genes with non-synonymous SNPs that significantly interacts with other loci on chromosomes 4, 11 and 18. Mechanistically, the absence of HNF1alpha in diabetic-prone (sensitive) strains leads to postnatal defective islets growth that is remarkably restored in resistant strains. Our findings are relevant to human genetics since Moda1 is syntenic with a human locus identified by genome wide association studies of fasting glycemia in patients. Most importantly, our results show that a single genetic locus can completely suppress diabetes in Hnf1a-deficiency.
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Registered trials
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