The Stimulation by Insulin of Amino Acid Uptake and Protein Synthesis in the Isolated Fetal Rat Heart

Clark, jr. C.M.

doi:10.1159/000240431

Cited by 16 publications

(1 citation statement)

References 8 publications

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“…The fetal heart is an insulin-responsive tissue [ 47 , 48 ] and it has long been hypothesized that elevated fetal insulin induced by maternal diabetes may contribute to fetal cardiac overgrowth [ 1 ]. Insulin signaling contributes to both embryonic and postnatal cardiac growth [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Maternal Hyperglycemia Directly and Rapidly Induces Cardiac Septal Overgrowth in Fetal Rats

Gordon

Reinking

et al. 2015

Journal of Diabetes Research

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Cardiac septal overgrowth complicates 10–40% of births from diabetic mothers, but perplexingly hyperglycemia markers during pregnancy are not reliably predictive. We thus tested whether fetal exposure to hyperglycemia is sufficient to induce fetal cardiac septal overgrowth even in the absence of systemic maternal diabetes. To isolate the effects of hyperglycemia, we infused glucose into the blood supply of the left but not right uterine horn in nondiabetic pregnant rats starting on gestational day 19. After 24 h infusion, right-sided fetuses and dams remained euglycemic while left-sided fetuses were moderately hyperglycemic. Echocardiograms in utero demonstrated a thickened cardiac septum among left-sided (glucose-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 glucose-derived anabolism were not different between sides. However, left-sided fetuses exhibited higher serum insulin and greater JNK phosphorylation compared to controls. These results show that hyperglycemic exposure is sufficient to rapidly induce septal overgrowth even in the absence of the myriad other factors of maternal diabetes. This suggests that even transient spikes in glucose may incite cardiac overgrowth, perhaps explaining the poor clinical correlation of septal hypertrophy with chronic hyperglycemia.

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