Abstract
Maternal diabetes can induce a number of developmental abnormalities in both laboratory animals and humans, including neural tube defects and facial deformities. The incidence of birth defects in newborns of diabetic women is approximately 3 to 5 times higher than among non-diabetics. In mice, non specific activation of the maternal immune system can reduce fetal birth defects caused by diverse etiologies, including diabetes induced craniofacial shortening and neural tube defects. This study was conducted to determine whether non-specific maternal immune stimulation could reduce diabetes induced orofacial clefts as well. Maternal immune function was stimulated prior to induction of hyperglycemia by one of three methods: maternal footpad injection with FCA; or maternal IP injection with GM-CSF; or maternal IP injection with IFNγ. Streptozocin (200 mg/kg IP) was then used to induce hyperglycemia (26–35 mmol blood glucose) in female ICR mice prior to breeding. Fetuses from 12–18 litters per treatment group, (over 100 fetuses per group) were collected at day 17 of gestation. Orofacial defects, although uncommon, were observed in fetuses from all groups, and consisted of cleft lip (cheiloschisis), cleft palate, and severe clefting of the lip, palate and upper jaw (cheilognathouranoschisis). However, unlike diabetes induced neural tube defects and craniofacial shortening, maternal stimulation with IFNγ, GM-CSF or FCA did not reduce the incidence or severity of facial clefts. Supported by NIH NCRR grant # K01RR16241-01A1
Published Version
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