» Articles » PMID: 23653578

Diabetic Embryopathy: a Developmental Perspective from Fertilization to Adulthood

Overview
Journal Mol Syndromol
Date 2013 May 9
PMID 23653578
Citations 15
Authors
Affiliations
Soon will be listed here.
Abstract

Maternal diabetes mellitus is one of the strongest human teratogens. Despite recent advances in the fields of clinical embryology, experimental teratology and preventive medicine, diabetes-related perturbations of the maternofetal unit maintain a considerable impact on the Healthcare System. Classic consequences of prenatal exposure to hyperglycemia encompass (early) spontaneous abortions, perinatal death and malformations. The spectrum of related malformations comprises some recurrent blastogenic monotopic patterns, i.e. holoprosencephaly, caudal dysgenesis and oculoauriculovertebral spectrum, as well as pleiotropic syndromes, i.e. femoral hypoplasia-unusual face syndrome. Despite this, most malformed fetuses display multiple blastogenic defects of the VACTERL type, whose (apparently) casual combination preclude recognizing recurrent patterns, but accurately testifies to their developmental stage at onset. With the application of developmental biology in modern medicine, the effects of diabetes on the unborn patient are expanded to include the predisposition to develop insulin resistance in adulthood. The mechanisms underlying the transgenerational correlation between maternal diabetes and proneness to adult disorders in the offspring remain unclear, and the epigenetic plasticity may represent the missing link. In this scenario, a development-driven summary of the multifaced consequences of maternal diabetes on fertility and child health may add a practical resource to the repertoire of available information on early stages of embryogenesis.

Citing Articles

A zebrafish model of nicotinamide adenine dinucleotide (NAD) deficiency-derived congenital disorders.

Tsurho V, Gilliland C, Ensing J, Vansickle E, Lanning N, Mark P bioRxiv. 2025; .

PMID: 39829932 PMC: 11741431. DOI: 10.1101/2025.01.10.632366.


The landscape of fetus metabolism in maternal hyperglycemia.

Kelly M, Martinez T, Jang C Trends Endocrinol Metab. 2024; 35(4):282-284.

PMID: 38341338 PMC: 11070186. DOI: 10.1016/j.tem.2024.01.012.


Pharmacological Action of Baicalin on Gestational Diabetes Mellitus in Pregnant Animals Induced by Streptozotocin via AGE-RAGE Signaling Pathway.

Qiu S, Wu X, Wu Q, Jin X, Li H, Roy R Appl Biochem Biotechnol. 2023; 196(3):1636-1651.

PMID: 37436545 DOI: 10.1007/s12010-023-04586-8.


Maternal diabetes negatively impacts fetal health.

Gonzalez Corona C, Parchem R Open Biol. 2022; 12(9):220135.

PMID: 36128718 PMC: 9490340. DOI: 10.1098/rsob.220135.


NAD+ deficiency in human congenital malformations and miscarriage: A new model of pleiotropy.

Mark P Am J Med Genet A. 2022; 188(9):2834-2849.

PMID: 35484986 PMC: 9541200. DOI: 10.1002/ajmg.a.62764.


References
1.
Miller J, Williamson E, Glue J, Gordon Y, Grudzinskas J, Sykes A . Fetal loss after implantation. A prospective study. Lancet. 1980; 2(8194):554-6. DOI: 10.1016/s0140-6736(80)91991-1. View

2.
Davis E, Peck J, Thompson D, Wild R, Langlois P . Maternal diabetes and renal agenesis/dysgenesis. Birth Defects Res A Clin Mol Teratol. 2010; 88(9):722-7. DOI: 10.1002/bdra.20702. View

3.
Pani L, Horal M, Loeken M . Rescue of neural tube defects in Pax-3-deficient embryos by p53 loss of function: implications for Pax-3- dependent development and tumorigenesis. Genes Dev. 2002; 16(6):676-80. PMC: 155364. DOI: 10.1101/gad.969302. View

4.
Pedersen J . Congenital malformations: the possible role of diabetes care outside pregnancy. Ciba Found Symp. 1978; (63):265-71. DOI: 10.1002/9780470720462.ch13. View

5.
Castori M, Rinaldi R, Capocaccia P, Roggini M, Grammatico P . VACTERL association and maternal diabetes: a possible causal relationship?. Birth Defects Res A Clin Mol Teratol. 2008; 82(3):169-72. DOI: 10.1002/bdra.20432. View