Amador A G, Bartke A, Beamer W G, Siler-Khodr T M
Department of Physiology, School of Medicine, Southern Illinois University, Carbondale 62901-6512.
Endocrinol Exp. 1988 Jun;22(2):87-97.
The autoregulation of testicular LH receptors was studied in mutant mice with congenital PRL and GH deficiency (df/df) and in mutant mice with congenital resistance to GH (pg/pg). Low dose of hCG produced an increase in LH receptors in df/df mice, but not in normal mice of the same strain. Intermediate doses of hCG did not affect LH receptors in df/df mice, while decreasing them in normal mice. In pg/pg mice, hCG caused changes in LH receptors which were identical to those observed in their normal siblings. Comparison of these two mutations suggests a lack of involvement of GH in the regulation of testicular LH receptors. Moreover, results obtained from df/df mice could indicate the presence of direct effects of the df mutation on testicular LH receptors.
在患有先天性催乳素和生长激素缺乏症的突变小鼠（df/df）以及先天性生长激素抵抗的突变小鼠（pg/pg）中研究了睾丸促黄体生成素（LH）受体的自身调节。低剂量的人绒毛膜促性腺激素（hCG）使df/df小鼠的LH受体增加，但同一品系的正常小鼠未出现这种情况。中等剂量的hCG对df/df小鼠的LH受体没有影响，却使正常小鼠的LH受体减少。在pg/pg小鼠中，hCG引起的LH受体变化与其正常同胞中观察到的变化相同。对这两种突变的比较表明，生长激素不参与睾丸LH受体的调节。此外，从df/df小鼠获得的结果可能表明df突变对睾丸LH受体有直接影响。
