Related Experiment Video
Updated: Aug 19, 2026
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Effect of premature birth and survival on hepatic thyroxine 5'-monodeiodinase activity in baboons
D S Lewis1, D DeChant, R A deLemos
1Department of Physiology and Medicine, Southwest Foundation for Biomedical Research, San Antonio, Texas 78228-0147.
Insights
Premature baboons show delayed thyroid hormone levels but their hepatic 5'-monodeiodinase type I (5'-MDI) activity matures postnatally. This suggests premature birth doesn't hinder 5'-MDI maturation despite initial hormone deficiencies.
Area of Science:
- Endocrinology
- Developmental Biology
- Perinatology
Background:
- Premature birth impacts neonatal thyroid hormone homeostasis.
- Hepatic 5 -monodeiodinase type I (5 -MDI) is crucial for thyroid hormone activation.
- Understanding 5 -MDI maturation in premature neonates is vital for clinical management.
Purpose of the Study:
- To investigate plasma thyroid hormones and hepatic 5 -MDI activity in a primate model of premature birth.
- To assess the impact of premature delivery on the developmental trajectory of 5 -MDI activity.
- To determine if premature birth affects the postnatal maturation of hepatic 5 -MDI.
Main Methods:
- Measurement of plasma T3 and T4 levels in fetal, premature, and term infant baboons.
- Assay of hepatic 5 -MDI activity using dithiothreitol.
- Kinetic analysis of 5 -MDI to determine Vmax and Km values.
- Assessment of hepatic sulfhydryl groups in premature baboons.
Main Results:
- Prematurely delivered baboons exhibited delayed T3 and T4 surges and prolonged hypothyroxinemia.
- Hepatic 5 -MDI activity was significantly lower in fetal baboons but increased near term.
- Postnatal hepatic 5 -MDI activity in premature baboons increased within 6 days, reaching levels similar to near-term fetuses.
- Kinetic analysis indicated differences in Vmax but not Km for fetal versus premature 5 -MDI.
- No significant differences in hepatic sulfhydryl groups were observed between premature baboon groups.
Conclusions:
- Premature birth in baboons leads to transient deficiencies in thyroid hormones.
- Despite initial deficits, hepatic 5 -MDI activity demonstrates significant postnatal maturation.
- The findings suggest that premature birth does not impede the developmental maturation of hepatic 5 -MDI activity.
Abstract:
Plasma thyroid hormones and hepatic 5'-monodeiodinase type I (5'-MDI) activity were measured in a primate model of premature birth and survival. When prematurely delivered at 140 days (term gestation is 184 days), infant baboons developed hyaline membrane disease, had no surge in T3 and T4, temporarily developed hypothyroxinemia, and had extremely low T3 concentrations during the first 40 h of life. After 4 days, both plasma T4 and T3 levels progressively increased, but were still considerably lower at 16 days compared to those in normal term infants. Hepatic 5'-MDI activity was measured in the presence of dithiothreitol in fetal, premature, and infant baboons. Fetal baboons at 140 and 161 days gestation had 80% less 5'-MDI activity than term infants, but at 178-180 days gestation, near term, fetal hepatic 5'-MDI activity increased to levels similar to those in young adults. Interruption of in utero development by premature birth resulted in no change in hepatic 5'-MDI activity after 24 h, but within 6 days after delivery, hepatic 5'-MDI had significantly increased to levels observed in fetal baboons near term. Kinetic analysis revealed that fetal and premature 5'-MDI had different maximum velocities and similar apparent Km values. There was no significant difference in hepatic total, protein, or nonprotein sulfhydryl groups between 1- and 10-day-old premature (140 days gestation) baboons. These results suggest that premature birth does not limit the postnatal maturation of hepatic 5'-MDI activity.
Related Concept Videos
01:14Effect of Hepatic Disease on Pharmacokinetics: Active Drug, Metabolite and Fraction of Metabolized Drug
01:22Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test