Effect of Streptozotocin Administration to Pregnant Mice on Serum Glucose, Glycosylated Hemoglobin and Weight of Organs of the Mother Mice and Their Pups

Fujii, Emiko; Nomoto, Teruko

doi:10.1254/jjp.48.391

Cited by 5 publications

(1 citation statement)

References 15 publications

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“…Chemically‐induced type 1 diabetes can be achieved using streptozotocin (STZ), which is a toxin that causes specific destruction of the β‐cells in the islets of Langerhaans (Fujii and Nomoto, 1988). By varying the STZ concentration and exposure time, the degree and duration of type 1 diabetes can be manipulated in experimental animals (Rodrigues et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Fetal cardiac effects of maternal hyperglycemia during pregnancy

Corrigan

Brazil

McAuliffe

2009

Birth Defects Research

120

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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.

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Section: Discussionmentioning

confidence: 99%

Fetal cardiac effects of maternal hyperglycemia during pregnancy

Corrigan

Brazil

McAuliffe

2009

Birth Defects Research

120

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Experimental Mechanisms of Diabetic Embryopathy and Strategies for Developing Therapeutic Interventions

Zhao

Reece

2005

Journal of the Society for Gynecologic Investigation

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A high frequency of birth defects is seen in infants born to diabetic mothers. The mechanisms by which maternal hyperglycemia, the major teratogenic factor, induces embryonic malformations remain to be addressed. It has been shown that increases in programmed cell death are one of the factors causing embryonic malformations. Hyperglycemia-induced apoptosis is associated with oxidative stress, lipid peroxidation, and decreased antioxidant defense capacity in the embryos. Recent studies have revealed that mitogen-activated protein kinases as intracellular signaling factors are involved in hyperglycemia-induced embryopathy. Based on the findings, interventions to prevent embryonic malformations have been explored. Strategies include supplementation of molecules that are deficient in the embryos under hyperglycemic conditions and antioxidants to alleviate the adverse effects of oxidative stress. The ultimate goal is to develop multi-nutrient dietary supplements to eliminate embryonic abnormalities induced by maternal diabetes.

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