Hormonal regulation of androgen-binding protein in the rat.

Effects of gonadotropins and gonadal steroids on androgen-binding protein (ABP) production by the testis and its secretion into the blood and transport into the epididymis were studied in 20- and 30-day-old rats. These animals had been treated with hCG, FSH, the Nal-Glu GnRH antagonist [Ac-D2Nal1,D4ClDPhe2,D3Pal3,Arg5,DGlu6(AA) ,DAla10]LHRH (antagonist), testosterone propionate, or estradiol benzoate, alone or in combination, for 10 days before assessment of ABP. Antagonist administration suppressed the testicular content (nanograms per organ) of ABP to below control (untreated) levels in both age groups. When hCG or testosterone was given along with the antagonist, they overcame the effect of the antagonist, and the resultant ABP values exceeded untreated control levels in both the 20- and 30-day-old rats. Treatment of rats with these hormones in the absence of the GnRH antagonist also elevated the ABP content of the testis above that of untreated controls. FSH administered with antagonist was able to prevent the antagonist-induced suppression of testicular ABP content. When rats were treated with FSH alone, the content of ABP in the testis was increased above untreated control levels in the 30-day-old group, but not in the 20-day-old group. The simultaneous administration of FSH and hCG did not result in an increase in testicular ABP content above that caused by hCG or testosterone alone. The increase in the ABP content of the testis caused by FSH administration was only about one sixth that caused by hCG or testosterone. Since testosterone or hCG, even in the presence of antagonist, was able to maximally stimulate ABP production by the testis of both age groups, we conclude that testosterone is the major in vivo regulator of its synthesis. Only combined treatment with hCG and FSH was able to increase transport of ABP into the epididymis of 20-day-old rats. All treatments that increased the testicular content of ABP in the 30-day-old rats also increased its transport into the epididymis. Treatments that drastically reduced the content of ABP in the testis of 20-day-old rats (antagonist, estradiol, estradiol plus antagonist) also reduced ABP secretion into the serum. Only treatment with estradiol reduced the secretion of ABP into the serum of 30-day-old rats. None of the treatments increased the ABP secretion into the bloodstream above untreated control levels.