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It has been shown that hypothyroidism in the rat produces a prolongation of pregnancy associated with a delay in the fall of circulating progesterone (P 4 ) at term. The aim of the present work is to determine whether the delayed P 4 decline in hypothyroid mother rats is due to a retarded induction of P 4 degradation to 20αOH P 4 or to a stimulation of its synthesis, and to investigate the possible mechanisms that may underlie the altered luteal function. We determined by RIA the circulating profile of the hormones (TSH, PRL, LH, P 4 , PGF2α, and PGE2) involved in luteal regulation at the end of pregnancy and, by semiquantitative RT-PCR, the expression of factors involved in P 4 synthesis (CytP450scc, StAR, 3βHSD, PRLR) and metabolism (20αHSD, PGF2αR, iNOS and COX2). Our results show that the delay in P 4 decline and parturition is the resultant of retarded luteal regression, caused by a combination of decreases in luteolytic factors, mainly luteal PGF2α, iNOS mRNA expression and also circulating LH, and increased synthesis or action of luteotrophic factors, such as luteal and circulating PGE2 and circulating PRL. All these changes may be direct causes of the decreased 20αHSD mRNA and protein (measured by western blot analysis) expression, which in the presence of unchanged expression of the factors involved in P 4 synthesis results in elevated luteal and circulating P 4 that prolonged pregnancy and also may favor longer survival of the corpus luteum.

Hypothyroidism prolongs corpus luteum function in the pregnant rat