Effects of growth hormone and thyroxine on pituitary and testicular function in two types of hereditary dwarf mice.

Abstract

AbstractHereditary dwarf mice are growht hormone (GH)‐ and prolactin (PRL)‐deficient and hypothyroid. Administration of PRL, GH, or thyroxine (T4) can induce fertility inmale dwarf mice. The mechanism of action of PRL appears to involve stimulation of FSH release, increased ability of the testes to bind LH, and increased production of testosterone (T) and spermatozoa. To obtain some information on the action of GH and T4 on the pituitary‐testicular axis in these animals, we have examined spermaogenesis, plasma hormone levels, and testicular T production in vitro in Snell (dw) and Ames (df) dwarf mice treated with GH or T4. Treatment with T4 (2μg/day for 2 weeks; 1μg/day for 4 weeks or 4–6μg 3 ×/wk for 6 weeks) or with GH (125 μg/day for 2 weeks; or 38–150 μg/day for 4 weeks) increased body weight, stimulated spermatogenesis, and increased the weight of the testes and seminal vesicles. Treatment with T4 had no significant effects on plasma hormone levels, while treatment with GH for 2 weeks increased plasma levels of LH, FSH, and T in Ames but not in Snell dwarf mice. The ability of the testes to produce T in vitro in the presence of hCG was not affected by in vivo treatment with GH or T4 in either df or dw dwarf mice. These results indicate that the stimulatory effect of T4 and GH on testicular function of dwarf mice does not involve increased responsiveness to gonadotropins or major chages in gonadotropin release. Comparison of the present results with those obtained earlier with PRL indicates that the ability of PRL to induce fertility in dwarf mice may be a specific action of this hormone on the pituitary‐testicular axis, rather that a result of its inherent somatotropic activity.