Maternal XXXX Directly and Rapidly Induces Cardiac Septal Overgrowth in Fetal @entity35 .

@entity6 @entity1184 @entity6336 @entity413 @entity299 @entity35 @entity1602 @entity4854
Cardiac septal overgrowth complicates 10-40% of births from diabetic mothers, but perplexingly @entity4854 markers during pregnancy are not reliably predictive. We thus tested whether fetal exposure to @entity4854 is sufficient to induce fetal cardiac septal overgrowth even in the @entity6 . To isolate the effects of @entity4854 , we infused @entity413 into the blood supply of the left but not right uterine horn in nondiabetic pregnant @entity35 starting on gestational day 19. After 24   h infusion, right-sided fetuses and dams remained euglycemic while left-sided fetuses were moderately @entity1602 . Echocardiograms in utero demonstrated a thickened @entity299 among left-sided ( @entity413 -exposed, 0.592    0.016   mm) compared to right-sided (control, 0.482    0.016   mm) fetuses. Myocardial proliferation was increased 1.5    0.2-fold among left-sided compared to right-sided fetuses. Transcriptional markers of @entity413 -derived anabolism were not different between sides. However, left-sided fetuses exhibited higher serum insulin and greater @entity6336 phosphorylation compared to controls. These results show that @entity1602 exposure is sufficient to rapidly induce septal overgrowth even in the absence of the myriad other factors of maternal @entity6 . This suggests that even transient spikes in @entity413 may incite @entity299 , perhaps explaining the poor clinical correlation of @entity1184 with @entity4854 .
