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Hypothyroidism prolongs corpus luteum function in the pregnant rat

Laboratorio de Reproducción y Lactancia, IMBECU-CONICET, Mendoza, Argentina ¹ Laboratorio de Fisiopatologia Ovarica, CEFYBO-CONICET, Buenos Aires, Argentina

Correspondence should be addressed to G A Jahn, Laboratorio de Reproducción y Lactancia, IMBECU-CRICYT-CONICET, C.C. 855, 5500 Mendoza, Argentina; Email: gjahn{at}lab.cricyt.edu.ar, bhapon{at}lab.cricyt.edu.ar

It has been shown that hypothyroidism in the rat produces a prolongation of pregnancy associated with a delay in the fall of circulating progesterone (P₄) at term. The aim of the present work is to determine whether the delayed P₄ decline in hypothyroid mother rats is due to a retarded induction of P₄ degradation to 20OH P₄ 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, P₄, PGF2, and PGE2) involved in luteal regulation at the end of pregnancy and, by semiquantitative RT-PCR, the expression of factors involved in P₄ synthesis (CytP450scc, StAR, 3ßHSD, PRLR) and metabolism (20HSD, PGF2R, iNOS and COX2). Our results show that the delay in P₄ decline and parturition is the resultant of retarded luteal regression, caused by a combination of decreases in luteolytic factors, mainly luteal PGF2, 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 20HSD mRNA and protein (measured by western blot analysis) expression, which in the presence of unchanged expression of the factors involved in P₄ synthesis results in elevated luteal and circulating P₄ that prolonged pregnancy and also may favor longer survival of the corpus luteum.