Ontogeny of growth hormone and LH beta-, FSH beta- and alpha-subunit mRNA levels in the porcine fetal and neonatal anterior pituitary.

The mechanism underlying the ontogenetic increase in plasma growth hormone (GH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) concentration during fetal life in mammalian species and the prenatal sex difference in these hormones in some species is not fully understood. To this end anterior pituitaries were collected from German Landrace fetuses and piglets at day (d) 50, 65, 80, 95, 110 pc and d 6 pp and pituitary GH, LH beta, FSH beta and alpha-subunit mRNA levels were determined by measuring Northern blot hybridization signals. GH mRNA was detected in both sexes as early as d 50 pc. The mRNA level markedly increased with age in both sexes (males > females, P < or = 0.05) reaching its maximum at d 95/110 pc. LH beta mRNA signals were first detected at d 50 pc in females and at d 65 pc in males increasing thereafter to a maximum at d 6 pp in both sexes (P < or = 0.05). In males the augmentation in LH beta mRNA was delayed compared to females (P < or = 0.01). Before d 80 pc no FSH beta mRNA hybridization signals were apparent. Thereafter the mRNA level continuously increased with age (P < or = 0.01) in both sexes reaching its maximum at d 6 pp. The FSH beta mRNA level in females was always higher than in males (P < or = 0.01). As early as d 50 pc the alpha-subunit mRNA level was high in both sexes and further increased without sex difference to d 6 pp (P < or = 0.05). In conclusion, the mRNA levels of GH, LH beta and FSH beta are age and sex dependent during fetal development. We suggest that the fetal increase in plasma GH concentration can be accounted for by changes in GH mRNA levels, while the dramatic perinatal decrease in plasma GH concentration seems to be primarily controlled at the posttranslational and/or secretion level. The fetal sex difference and the increase in plasma LH and FSH concentrations seems to be primarily dependent on the cellular concentration of the gonadotropin beta-subunit mRNAs and/or number of gonadotrophs.