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Maternal Hyperglycemia (maternal + hyperglycemia)

Distribution by Scientific Domains

Life Sciences	80%

Selected Abstracts

Heart changes in 17-day-old fetuses of diabetic ICR (Institute of Cancer Research) mothers: Improvement with maternal immune stimulation

CONGENITAL ANOMALIES, Issue 1 2009
Juan Claudio Gutierrez
ABSTRACT Maternal diabetes mellitus is associated with increased fetal teratogenesis, including cardiovascular defects. Non-specific maternal immune stimulation with Freund's complete adjuvant (FCA) or interferon gamma (IFN,) has been associated with protection against birth malformations. Using a diabetic mouse model, late-gestation fetal heart and great vessel morphology were analyzed. Four groups of mice were used: non-diabetic females as a control group, hyperglycemic females induced by streptozotocin as a diabetic group, and diabetic females injected either with FCA or IFN,. At day 17 of gestation, females were euthanized and one fetus was arbitrarily selected per litter for fixation and sectioning. Treatment-induced changes in cardiac development were assessed from digital images of serial sections taken at standardized levels in the thorax. One-way parametric and non-parametric ANOVA and ordinal logistic regression were performed to compare the difference among groups (P < 0.05). Maternal hyperglycemia altered morphology of the late-gestation fetal mouse heart by causing ventricular chamber dilation, sectional myocardial reduction, and an increase in transversal aortic area. FCA protected the fetal heart from cavitary dilation in diabetic mothers. FCA and IFN, protected the fetal heart against reduction of myocardial area, and ascending thoracic aorta dilation. Consequences of late gestation heart chamber dilation and myocardial reduction are not yet known. Maternal immune stimulation partially protected against these developmental defects by mechanisms that remain unclear. [source]

Aortic and ventricular dilation and myocardial reduction in gestation day 17 ICR mouse fetuses of diabetic mothers

BIRTH DEFECTS RESEARCH, Issue 6 2007
J. Claudio Gutierrez
Abstract BACKGROUND: Maternal diabetes mellitus is associated with increased fetal teratogenesis, including cardiovascular defects. Information regarding cardiovascular changes in late-gestation fetal mice, related to maternal hyperglycemia, is not present in the literature. METHODS: Late-gestation fetal heart and great vessel morphology were analyzed in fetuses from control and diabetic mice. Female ICR mice were injected with streptozocin (200 mg/kg IP) prior to mating to induce diabetes (n = 8). Nonhyperglycemic females were used as controls (n = 8). At day 17 of gestation, females were euthanized and one fetus was arbitrarily selected per litter to analyze the heart and great vessels. Six additional fetuses from different litters, showing external malformations (spina bifida and/or exencephaly), were also evaluated from the diabetic group. Fetal thoraxes were processed using routine histopathologic techniques, and 7-,m transversal sections were stained with hematoxylin-eosin. Digital images of sections were made and analyzed using NIH Image J software to compare regional cardiac development. Student's t tests for means were performed to determine differences between groups (p < .05). RESULTS: Maternal hyperglycemia caused a dilation of late-gestation fetal ventricular chambers, a reduction of total ventricular myocardial area, and an increase in transversal ascending thoracic aortic area. Three of six fetuses that displayed external malformations showed an overt cardiac defect, beyond the ventricular and myocardial changes. CONCLUSIONS: Maternal hyperglycemia altered morphology of the late-gestation fetal mouse heart. Postnatal persistence or consequences of late-gestation heart chamber dilation and myocardial reduction are not yet known. Birth Defects Research (Part A) 2007. © 2007 Wiley-Liss, [source]

Doppler sonographic characteristics of umbilical and uterine arteries during oral glucose tolerance testing in healthy pregnant women

JOURNAL OF CLINICAL ULTRASOUND, Issue 9 2003
Yariv Yogev MD
Abstract Purpose Studies have shown that maternal hyperglycemia may be associated with increased placental resistance to blood flow and possibly adverse perinatal outcomes. The aim of this study was to determine whether Doppler velocimetric dynamics change in the uterine and umbilical arteries in healthy pregnant women (without gestational diabetes) during acute hyperglycemia induced by oral glucose tolerance testing. Methods Flow in the umbilical and right and left uterine arteries was assessed by spectral Doppler sonographic examination of healthy pregnant women at 24,28 weeks' menstrual age. Four Doppler studies were conducted for each woman: 1 before oral administration of 100 g of glucose and 3 more at 1, 2, and 3 hours after glucose administration. The systolic-to-diastolic ratio was calculated for the umbilical artery, and the resistance index was calculated separately for the left and right uterine arteries. Results All results of oral glucose tolerance testing were normal, and Doppler signals were obtained in all 30 patients enrolled. No abnormal systolic-to-diastolic ratios or resistance indices were detected in any of the examinations. No significant differences in waveforms or resistance indices between the right and left uterine arteries were found during the various testing intervals. Conclusions Acute hyperglycemia induced in healthy pregnant women does not affect blood flow velocimetric characteristics in the umbilical or uterine arteries at any stage of oral glucose tolerance testing. © 2003 Wiley Periodicals, Inc. J Clin Ultrasound 31:461,464, 2003 [source]

Fetal cardiac effects of maternal hyperglycemia during pregnancy

BIRTH DEFECTS RESEARCH, Issue 6 2009
Niamh Corrigan
Maternal diabetes mellitus is associated with increased teratogenesis, which can occur in pregestational type 1 and type 2 diabetes. Cardiac defects and with neural tube defects are the most common malformations observed in fetuses of pregestational diabetic mothers. The exact mechanism by which diabetes exerts its teratogenic effects and induces embryonic malformations is unclear. Whereas the sequelae of maternal pregestational diabetes, such as modulating insulin levels, altered fat levels, and increased reactive oxygen species, may play a role in fetal damage during diabetic pregnancy, hyperglycemia is thought to be the primary teratogen, causing particularly adverse effects on cardiovascular development. Fetal cardiac defects are associated with raised maternal glycosylated hemoglobin levels and are up to five times more likely in infants of mothers with pregestational diabetes compared with those without diabetes. The resulting anomalies are varied and include transposition of the great arteries, mitral and pulmonary atresia, double outlet of the right ventricle, tetralogy of Fallot, and fetal cardiomyopathy. A wide variety of rodent models have been used to study diabetic teratogenesis. Both genetic and chemically induced models of type 1 and 2 diabetes have been used to examine the effects of hyperglycemia on fetal development. Factors such as genetic background as well as confounding variables such as obesity appear to influence the severity of fetal abnormalities in mice. In this review, we will summarize recent data on fetal cardiac effects from human pregestational diabetic mothers, as well as the most relevant findings in rodent models of diabetic cardiac teratogenesis. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. [source]