Endocrine Abstracts

Type I 5'-monodeiodinase (5'-MDI) converts thyroxine (T₄) to triiodothyronine (T₃). In fetal sheep, hepatic 5'-MDI activity increases near term in association with the prepartum cortisol surge. This study investigated the effect of maternal dexamethasone treatment, in clinically relevant doses, on hepatic and renal type I 5'-MDI activity and plasma thyroid hormone concentrations in fetal sheep.

From 125 days of gestation (term 145 plus/minus 2 days), nine ewes, carrying single fetuses, were injected twice i.m. with either saline (0.9% NaCl, n=4) or dexamethasone (2x12 mg in 2 ml 0.9% NaCl, n=5) at 24 hour intervals. Ten hours after the second injection, the ewes and fetuses were euthanised, and tissues and umbilical arterial blood were collected. Plasma T₄ and T₃ were measured by radioimmunoassay, and tissue type I 5'-MDI activity by outer ring deiodination of iodinated reverse-T₃. Data (mean plus/minus SEM) were analysed by unpaired t-test and linear regression.

Fetal plasma T₃ but not T₄ concentrations were increased by maternal dexamethasone treatment (p<0.001). Hepatic type I 5'-MDI activity in the dexamethasone-exposed fetuses (2308 plus/minus 112 pmoles I^-/mg protein/hour) was greater than in the control fetuses (1188 plus/minus 40, p<0.001). Overall, plasma T₃ correlated with hepatic type I 5'-MDI activity (r=0.96, p<0.001). There was no significant difference in renal type I 5'-MDI activity between the saline (29.1 plus/minus 4.9 pmoles I^-/mg protein/hour) and dexamethasone-exposed fetuses (35.3 plus/minus 4.1).

Therefore, maternal dexamethasone treatment increases hepatic type I 5'-MDI and plasma T₃ concentration in fetal sheep. Changes in T₃ bioavailability may mediate some of the maturational effects of dexamethasone in the preterm fetus.

Supported by the BBSRC and Tommy's, the baby charity.