NORMAL SERUM T3 POSTNATAL SURGE AND INCREASED REVERSE T3 LEVELS IN SELENIUM-DEFICIENT RAT PUPS

Abstract

In adult rats, selenium (Se) deficiency markedly decreases liver type I outer-ring 5′ deiodinase (5′D-I, a selenoenzyme convening T4 into T3), resulting in a 40% increase in serum T4 concentrations. Serum T3 and reverse T3 (rT3) concentrations are unchanged or marginally decreased or increased, respectively. In rat fetuses, serum T4 and rT3 concentrations are not affected by selenium deficiency. We studied the effect of Se deficiency on thyroid function in the rat neonate. 28 weanling female rats were fed a Se replete (Se+) or Se deficient (Se−) diet for 4 wk prior to mating and throughout gestation. 2-3 pups from each litter were sacrificed 7, 14 and 21 days after delivery. Serum T4, T3, rT3 and TSH concentrations and liver 5′D-I activity, to assess Se deficiency, were measured.*P<0.001 compared to corresponding Se+group Mean(SE).In Se- pups, the decrease in 5′D-I activity was >89% confirming Se deficiency (P<0.001). In contrast to adult rats, Se deficiency causes no increase in serum T4 in 1 and 2 wk old pups and only a 20% increase in 3 wk old pups, but results in a 60-250% increase in serum rT3.Conclusion: 1) In the rat neonate, the 500 to 600% surge in serum T3 levels observed physiologically after birth is independent of liver 5′D-I activity, strongly suggesting that T4 to T3 conversion by peripheral tissues is not a major source of T3 in the neonate; 2) In contrast, serum rT3 levels increase markedly in Se- pups as early as the 7th postnatal day, suggesting that liver 5′D-I is important in rT3 metabolism.