ArticleDiabetologia2004
Hyperglycaemia potentiates the teratogenicity of retinoic acid in diabetic pregnancy in mice.
Article in Diabetologia, 2004. 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, 16 citations in OpenAlex.
- Hyperglycemia alters retinoic acid catabolism in embryos exposed to a maternal diabetic milieu.PloS one · 2023Article
- Phenotypic Screening for Small Molecules that Protect β-Cells from Glucolipotoxicity.ACS chemical biology · 2022Article
- Perosomus elumbis in a stillborn rhesus macaque (Macaca mulatta): A case report.Journal of medical primatology · 2020Article
- Perturbation of Retinoid Homeostasis Increases Malformation Risk in Embryos Exposed to Pregestational Diabetes.Diabetes · 2017Article
- MBTPS1/SKI-1/S1P proprotein convertase is required for ECM signaling and axial elongation during somitogenesis and vertebral development†.Human molecular genetics · 2015Article
- Hyperglycemia induces embryopathy, even in the absence of systemic maternal diabetes: an in vivo test of the fuel mediated teratogenesis hypothesis.Reproductive toxicology (Elmsford, N.Y.) · 2014Article
- Understanding diabetic teratogenesis: where are we now and where are we going?Birth defects research. Part A, Clinical and molecular teratology · 2010Review
- Wnt signaling in caudal dysgenesis and diabetic embryopathy.Birth defects research. Part A, Clinical and molecular teratology · 2008Article
- Hyperglycemia: its imminent effects on mammalian nephrogenesis.Pediatric nephrology (Berlin, Germany) · 2005Review
- Efficacy of Spirulina platensis in improvement of the reproductive performance and easing teratogenicity in hyperglycemic albino mice.Indian journal of pharmacologyArticle
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisWe recently showed in mice that maternal diabetes increases embryonic susceptibility to caudal regression induced by vitamin A metabolite retinoic acid. Here we tested whether in the maternal diabetic milieu hyperglycaemia is the critical factor responsible for mediating this increased susceptibility.
methodsNon-diabetic pregnant mice were made hyperglycaemic by subcutaneous injections of glucose at regular intervals. Conversely, diabetic pregnant mice were treated with phlorizin to induce renal glucosuria and thus reduce blood glucose concentrations. Pregnant mice were treated with retinoic acid and the extent of caudal regression in mouse embryos, measured in terms of the ratio of tail length to crown-rump length was assessed. Embryos were also examined for Wnt-3a expression and cell death.
resultsEmbryos of mice treated with glucose had a greater extent of caudal regression induced by retinoic acid than saline-treated controls, with enhanced down-regulation of Wnt-3a expression and exacerbated cell death specifically at the caudal end of the embryo. Embryos of diabetic mice treated with phlorizin had a similar extent of caudal regression to embryos of non-diabetic mice after treatment with retinoic acid. CONCLUSIONS/
interpretationHyperglycaemia increases embryonic susceptibility to caudal regression induced by retinoic acid, with the underlying cellular and molecular changes closely mimicking those that occur in maternal diabetes. Reduction of blood glucose concentrations in diabetic mice completely abolishes this increased susceptibility to retinoic acid. These results suggest that in maternal diabetes hyperglycaemia is the critical factor responsible for potentiating the teratogenic effect of retinoic acid.
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