ArticleScientific reports2017
Absence of a gestational diabetes phenotype in the LepRdb/+ mouse is independent of control strain, diet, misty allele, or parity.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 30 citations in OpenAlex.
- Higher weight in partially leptin-resistant db/+ mice is associated with positive effects on bone.The Journal of endocrinology · 2023Article
- Mouse Models of Gestational Diabetes Mellitus and Its Subtypes: Recent Insights and Pitfalls.International journal of molecular sciences · 2023Review
- RBM15 suppresses hepatic insulin sensitivity of offspring of gestational diabetes mellitus mice via m6A-mediated regulation of CLDN4.Molecular medicine (Cambridge, Mass.) · 2023Article
- A fresh look to the phenotype in mono-allelic likely pathogenic variants of the leptin and the leptin receptor gene.Molecular and cellular pediatrics · 2021Review
- Vitamin B6 deficiency disrupts serotonin signaling in pancreatic islets and induces gestational diabetes in mice.Communications biology · 2021Article
- Assessment of autism-relevant behaviors in C57BKS/J leptin receptor deficient mice.Hormones and behavior · 2021Article
- Exploring the causes and consequences of maternal metabolic maladaptations during pregnancy: Lessons from animal models.Placenta · 2020Review
- Leprdb/+ Dams Protect Wild-type Male Offspring Bone Strength from the Detrimental Effects of a High-Fat Diet.Endocrinology · 2020Article
- Pregnancy in human IAPP transgenic mice recapitulates beta cell stress in type 2 diabetes.Diabetologia · 2019Article
- Programming of Vascular Dysfunction in the Intrauterine Milieu of Diabetic Pregnancies.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treatment options for gestational diabetes (GDM) are limited. In order to better understand mechanisms and improve treatments, appropriate animal models of GDM are crucial. Heterozygous db mice (db/+) present with glucose intolerance, insulin resistance, and increased weight gain during, but not prior to, pregnancy. This makes them an ideal model for GDM. However, several recent studies have reported an absence of GDM phenotype in their colony. We investigated several hypotheses for why the phenotype may be absent, with the aim of re-establishing it and preventing further resources being wasted on an ineffective model. Experiments were carried out across two laboratories in two countries (New Zealand and China), and were designed to assess type of control strain, diet, presence of the misty allele, and parity as potential contributors to the lost phenotype. While hyperleptinemia and pre-pregnancy weight gain were present in all db/+mice across the four studies, we found no consistent evidence of glucose intolerance or insulin resistance during pregnancy. In conclusion, we were unable to acquire the GDM phenotype in any of our experiments, and we recommend researchers do not use the db/+ mouse as a model of GDM unless they are certain the phenotype remains in their colony.
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