Hasegawa R, Eisenberg F
Proc Natl Acad Sci U S A. 1981 Aug;78(8):4863-6. doi: 10.1073/pnas.78.8.4863.
myo-Inositol biosynthesis has been examined in hypophysectomized and thyroidectomized male rats. After hypophysectomy, inositol-1-phosphate synthase [1L-myo-inositol-1-phosphate lyase (isomerizing), EC 5.5.1.4] in the reproductive organs and liver decreased markedly. At the same time, testicular acid phosphatase [orthophosphoric-monoester, phosphohydrolase (acid optimum), EC 3.1.3.2] and beta-glucuronidase (beta-D-glucuronide glucuronosohydrolase, EC 3.2.1.31) increased. Thyroidectomy caused a similar decrease in inositol-1-phosphate synthase in the liver but not in the reproductive organs. Follicle-stimulating in the liver but not in the reproductive organs. Follicle-stimulating hormone (follitropin) and luteinizing hormone (lutropin) restored the activity to at least normal levels in the testis, prostate, and seminal vesicle but not in the liver of hypophysectomized animals. Triiodothyronine and thyroxine stimulated liver synthase 30-fold in hypophysectomized animals. We conclude that inositol-1-phosphate synthase in the reproductive organs is under more or less direct control of the pituitary; in the liver, the control is mediated through the thyroid.
已对垂体切除和甲状腺切除的雄性大鼠的肌醇生物合成进行了研究。垂体切除后,生殖器官和肝脏中的肌醇-1-磷酸合酶[1L-肌醇-1-磷酸裂解酶(异构化),EC 5.5.1.4]显著降低。与此同时,睾丸酸性磷酸酶[正磷酸单酯,磷酸水解酶(最适酸性),EC 3.1.3.2]和β-葡萄糖醛酸酶(β-D-葡萄糖醛酸葡萄糖苷水解酶,EC 3.2.1.31)增加。甲状腺切除导致肝脏中肌醇-1-磷酸合酶出现类似下降,但生殖器官中未出现。促卵泡激素和促黄体生成素使垂体切除动物的睾丸、前列腺和精囊中的活性恢复到至少正常水平,但肝脏中未恢复。三碘甲状腺原氨酸和甲状腺素在垂体切除动物中使肝脏合酶活性提高了30倍。我们得出结论,生殖器官中的肌醇-1-磷酸合酶或多或少受垂体直接控制;在肝脏中,这种控制是通过甲状腺介导的。