Abstract
I's role via its R in the brain, unlike other organs is unknown. Hypothyroidism(HP) influences fetal(F) lung and liver IR and retards B metabolism. The ontogeny of B IR in plasma membranes(PM) was examined to explore the role of I in rabbit F(30d.) and newborn(N) B (1d, 6d). Groups with PTU-induced HP(F and N), N with T4 corrected HP (ET) and hyperthyroidism(HT) were also studied. Specific 125I-I binding/200μg BPM (IB), IR no.×1010mg prot.-1 and affinity (Kē×108=0.91±.08) were determined. (UD=undetectable, p < .01 vs. control (C)).
Brain DNA did not change, IR no. expressed/DNA revealed similar trends. (Preliminary culture studies revealed specific IB to isolated 1d N neurons). We suggest that the NB IR changes induced by ↑ or ↓ by T4 in part mediate the changes in B metabolism, the fetus being unresponsive.
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Devaskar, S., Holkamp, N., Marino, N. et al. THYROIDAL STATUS MODULATES THE INSULIN(I) RECEPTOR (R) CHARACTERISTICS OF THE DEVELOPING BRAIN(B). Pediatr Res 18 (Suppl 4), 137 (1984). https://doi.org/10.1203/00006450-198404001-00262
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DOI: https://doi.org/10.1203/00006450-198404001-00262