Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D06457 (HCG)
 2,659 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year-old man was admitted to the Urological Department of Tokyo University, with complaints of delayed puberty and growth retardation. At the age of 14 years, he found his skeletal growth retarded. Since then he had not shown any development of secondary sex characters, such as change of voice, appearance of public and axillary hair and development of external genital organs. He had not experienced the ejaculation and libido, while the excretion has been maintained. This feminized patient showed poorly developed external genitalia, while there was no evidence of galactorrhea or gynecomastia. Ophthalmologic examinations were normal. Endocrinological studies revealed moderate hyperprolactinemia (185-200 ng/ml) and marked disorder for GH secretion. Gonadotropins were low normal and their responses to LH-RH were moderately disturbed. Serum testosterone level was extremely low and its responses to HCG were insufficient. Under the diagnosis of prolactinoma, he was referred to the Neurological Department. Plain skull film and tomography of the sella showed a deformed and slightly expanded sella, the measurement of which were within normal limits. No supra-sellar extention was demonstrated by pneumoencephalography and CT scan. A diagnosis of PRL producing microadenoma was made, and a radical removal of the tumor was performed through the transsphenoidal route. In most tumor cells the presence of PRL was revealed by immunohistochemical stains. Postoperatively, PRL levels returned to normal, while other hormonal deficiencies remained unchanged. With the administration of testosterone, he gradually became masculine and reportedly gained normal libido and potency.
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PMID:[Male prolactin producing pituitary microadenoma -a case report (author's transl)]. 706 99

In this paper, we revealed the changes in maternal plasma concentration of PRL, HCG, HPL, progesterone (P), estradiol-17 beta (E2), estriol (E3), estetrol (E4) and dehydroepiandrosterone-sulfate (DHEA-S) after the administration of bromocriptine during pregnancy. Blood samples were collected from 23 women with gestation ranging from 7 to 28 weeks. Sixteen patients had therapeutic abortion and other 7 patients had inevitable abortion. PRL, HCG, HPL, P, E2, E3, E4 and DHEA-S were measured by radioimmunoassay. The PRL decreased significantly at 120 and 180 minutes after the administration of bromocriptine in any case. In 4 cases out of 10 cases in early normal pregnancy, plasma E2 level decreased to 50% lower than the basal level, but no significant change of E2 occurred after bromocriptine in early and mid pregnancy. Bromocriptine made no change in HCG, HPL, P, E3, E4 and DHEA-S for any group. Our data suggested that bromocriptine had effect on only plasma PRL level, and this drug or the change of PRL level had no effect on P, estrogen, DHEA-S, HPL and HCG concentration during pregnancy.
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PMID:[Effect of bromocriptine on the endocrine profile during pregnancy]. 717 75

Several reports have revealed that human prolactin increases during pregnancy, not only in maternal and fetal serum but also in the amniotic fluid. The source and the role of prolactin in the amniotic fluid however, have not been clear up to now. In their incubation experiment, Riddick et al (29) proved that decidual tissue at term could secret immunoreactive prolactin (IR-PRL). In order to investigate the source of PRL in the amniotic fluid, we extracted IR-PRL from decidual or villous tissue in early normal pregnancies and measured it by a double antibody radioimmunoassay in this experiment. The results were the following: 1) We were able to measure IR-PRL from decidual or villous tissue in early pregnancy, the dilution curve of which paralleled pituitary standard prolactin. The cross reaction of a PRL standard preparation with HCG and HPL was not recognized within 10 micrograms/ml. 2) In human decidual tissue, the IR-PRL concentration began to increase at about the sixth week, arrived at the peak value, 81.06 +/- 2.13 ng/0.1 g dry weight (d.w.) in the eighth week, and did not change significantly after that. In human villous tissue, although the IR-PRL concentration was distinctly lower than it was in the decidual tissue, it increased gradually and reached the level of 37.44 +/- 7.16 ng/0.1g d.w. in the tenth week. 3) The extracted material (IR-PRL) from these two tissues in the 8th week, amniotic fluid at term, and pituitary standard PRL were passed through a Sephadex G-100 column (2 X 93 cm) with phosphate buffer and saline (0.01M, PH 7.4). In the chromatogram of these four test materials, one peak of IR-PRL was observed. The peak of IR-PRL of decidual and villous tissues and amniotic fluid revealed almost the same fraction number but elevated after the pituitary PRL preparation. 4) By gel filtration, the IR-PRL was able to be differentiated from HCG but not from HPL. The peak of HCG appeared earlier than the peak of IR-PRL and HPL. 5) The distribution of IR-PRL between human decidual and villous tissues was significantly different from that of HPL. IR-PRL concentration was higher in the decidual tissue than in the villous tissue, while HPL concentration was higher in the villous tissue than it was in the decidual tissue. From this observation, we could consider that the sources of these two hormones were different. The results of these experiments suggest that one of the sources of PRL in the amniotic fluid was the decidual tissue.
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PMID:[A measurement of immunoreactive prolactin in the decidual and villous tissues of early pregnancy, and a comparison with the prolactin in the amniotic fluid (author's transl)]. 735 86

A novel method of ovarian stimulation for IVF is reported. Endocrine-normal ovulatory women with a history of unsuccessful IVF attempts by means of a long protocol of a GnRH agonist/hMG regimen (L regimen) were studied. Ovaries were stimulated by the three regimens described below. The bromocriptine-rebound (BR) regimen consisted of bromocriptine (B) 2.5mg/day administered daily beginning on day 4 of the preceding cycle and buserelin acetate administered beginning in early high phase. Administration of B was discontinued in the low phase of the IVF cycle and daily administration of hMG was begun 7 days later. HCG was administered when dominant follicles reached 16-18 mm in diameter. The bromocriptine-continuous (BC) regimen was the same as the BR regimen, except that B was administered until the administration of hCG. The L regimen was the same as the BR regimen, except that no B was administered. The pregnancy rate per oocyte retrieval was significantly higher on the BR regimen (56% in 70 cycles) than the L regimen (33% in 46 cycles), and lowest on the BC regimen (29% in 7 cycles). The rate of fertilization and cleavage per oocyte and the proportion of morphologically-good embryos were significantly higher on the BR regimen (59.1% and 57.3%, respectively) than the L regimen (46.3% and 48.0%, respectively), and lowest on the BC regimen (49.0% and 41.7%, respectively). Serum PRL concentrations (ng/ml) at the time hMG was started were 14.9 +/- 1.5, 7.9 +/- 1.7 and 2.5 +/- 0.7 on the BR, L and BC regimens, respectively. The results of this study show that the BR regimen increases the developmental potential of oocytes and the pregnancy rate, probably because of increasing serum PRL levels to within the normal range.
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PMID:[A novel method of ovarian stimulation for in vitro fertilization (bromocriptine-rebound method) increases developmental potential of oocytes and pregnancy rate]. 856 52

Proliferin-related protein (PRP) was originally identified as an angiogenesis inhibitor in mouse placentas. Indeed, the tissue expression of PRP has mainly been documented in placentas. We report herein for the first time that PRP is expressed in male rat testes. Immunocytochemical and in situ hybridization results showed positive PRP immunostaining in Leydig cells. Immunofluorescent staining of PRP in the TM3 Leydig cell line indicates that PRP is located within the cytoplasm. The expression pattern of PRP in rat testis exhibited an age-related increase. HCG significantly up-regulated the level of expression of PRP in TM3 cells via the PKA pathway. To elucidate the function of PRP, experiments were conducted to examine the consequences of lentiviral-mediated RNA interference (RNAi) of PRP on testosterone production and expression of several genes involved in steroidogenesis. PRP silencing caused a decrease in HCG-stimulated testosterone production. In addition, PRP silencing attenuated the increase in PRLR mRNA following HCG stimulation. Moreover, the enhanced effect of PRL on HCG-induced testosterone production was also weakened following PRP silencing, indicating that PRP may be involved in PRL function through an effect on PRL receptor expression in response to stimuli. Taken together, these data suggest that PRP is regulated by HCG and plays roles in male reproduction, such as testosterone production.
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PMID:Expression of proliferin-related protein in testis and the biological significance in testosterone production. 2167 48


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