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Yamaguchi M. Miyake A. Regulation of mouse placental lactogen secretion by factors secreted from the pituitary in vitro. Eur J Endocrinol 1996;134:123–7. ISSN 0804–4643

The effect of factors secreted from the pituitary on mouse placental lactogen I (mPL-I) and mPL-II secretion in vitro was examined. Co-culture of mouse placental cells from day 7 of pregnancy with the pituitary cells of the mother significantly stimulated mPL-I secretion but did not regulate mPL-II secretion. The effect on mPL-I secretion was dependent on the number of pituitary cells. The conditioned medium of pituitary cells also significantly stimulated mPL-I secretion but did not regulate mPL-II secretion. The stimulatory effect of mPL-I secretion was dependent on the volume of the conditioned medium. The number of cells containing mPL-I assessed by immunocytochemistry was increased by the co-culture in a cell number-dependent manner. Northern blot analysis for mPL-I indicated that treatment of placental cells with the pituitary-conditioned medium results in an increase of mPL-I gene expression. These findings suggest that factors secreted from the pituitary directly regulate mPL-I secretion, but not mPL-II secretion, before midpregnancy in vivo.

Masaaki Yamaguchi, Department of Obstetrics and Gynecology. Osaka University Medical School, 2-2 Yamadaoka, Suita. Osaka 565, Japan

Yamaguchi M, Fujii M, Miyake A. Cyclic AMP regulator expression of activin and inhibin subunit mRNAs in the mouse placenta and decidua. Eur J Endocrinol 1996;135:379–81. ISSN 0804–4643

We examined whether cAMP regulates expression of activin/inhibin subunit mRNAs in the mouse placenta and decidua. 8-Bromo-cAMP inhibited expression of inhibin α-subunit mRNA but stimulated expression of activin/inhibin β_A- and β_B-subunit mRNAs in placenta and decidua by the 3rd day of culture. Forskolin and cholera toxin also regulated expression of activin/inhibin subunit mRNAs in the same manner. However, activin-A did not affect expression of activin/inhibin subunit mRNAs. These findings suggest that cAMP inhibits inhibin production but stimulates activin production in the mouse placenta and decidua.

Masaaki Yamaguchi, Department of Obstetrics and Gynecology, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka, 565, Japan

Yamaguchi M, Kawai M, Kishi K, Miyake A, Regulation of rat placental lactogen (rPL)-II secretion: cAMP inhibits rPL-II secretion in vitro. Eur J Endocrinol 1995;133:342–6. ISSN 0804–4643

We examined whether epidermal growth factor (EGF), interleukin (IL)-1, IL-6 and cAMP analogs, which regulate mouse placental lactogen II secretion, affect rat placental lactogen (rPL)-II secretion using a rat choriocarcinoma cell line, Rcho-1. EGF, IL-1 and IL-6 did not affect rPL-II secretion, but 8-bromo-cAMP and forskolin inhibited rPL-II secretion by the 8th day of culture. The effects were dose dependent and the lowest concentrations of 8-bromo-cAMP and forskolin that significantly inhibited rPL-II secretion were 125 and 5 μmol/l, respectively. Cholera toxin also inhibited rPL-II secretion. The reverse hemolytic plaque assay for rPL-II indicated that the cells releasing rPL-II in the culture were giant cells and that 8-bromo-cAMP decreased the number of rPL-II-releasing cells. Western blot analysis of rPL-II yielded a single band at approximately 24.5 K, and 8-bromo-cAMP treatment significantly reduced the band intensity. Northern blot analysis of rPL-II indicated that 8-bromo-cAMP also reduced rPL-II gene expression. These findings suggest that the increase of intracellular cAMP accumulation results in inhibition of rPL-II secretion by decreasing rPL-II gene expression and inhibiting giant cell differentiation.

Masaaki Yamaguchi, Department of Obstetrics and Gynecology, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan

ABSTRACT

The response of serum LH to exogenous oestrogen administration was studied in 5 patients with testicular feminization syndrome (TFS).

The serum LH levels were elevated in all the patients, while serum testosterone levels were within the normal male range. Serum FSH levels were elevated in 4 patients and normal in one patient. Intravenous administration of 100 μg of LH-RH provoked a further increase in both LH and FSH. Following intravenous injection of 20 mg of conjugated oestrogen (Premarin®), the LH levels were serially determined until 120 h in TFS patients, 5 normal males, and 10 normal females during the mid-follocular phase (D_7-9). Both TFS patients and normal males showed no LH release following oestrogen injection in contrast to normal females who displayed a significant increase in LH with a peak at 48 to 56 h after the injection.

These results seem to suggest that the insensitivity of the hypothalamus to androgen in TFS patients do not affect the sex differentiation of the hypothalamus. The possible role of oestradiol conversion from testosterone in the hypothalamus is discussed.

Abstract. The effect of hydrocortisone on the release of luteinizing hormone (LH) and LH-releasing hormone (LRH) in response to clomiphene citrate (clomiphene) were examined in a sequential double chamber perifusion system by perifusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were perifused in sequence with medium containing 5 × 10⁻⁶ m hydrocortisone, a significant release in LH (100– 150% increase, P < 0.01–P < 0.05) was observed 40 min after the administration of 3 × 10⁻⁸ mol clomiphene. Clomiphene had no effect on LH release from the pituitary when perifused in series with the MBH without basal hydrocortisone infusion. Administration of clomiphene did not cause a significant increase in LH from the pituitary perifused alone, with or without medium containing hydrocortisone. The concentration of LRH in the efflux was significantly increased 40 min after clomiphene administration when MBH was perifused with medium containing hydrocortisone, whereas clomiphene had no effect when perifused with medium only. These data indicate that hydrocortisone stimulates the effect of clomiphene on LRH release from the hypothalamus, which in turn induces LH release from the pituitary.

Abstract.

The effect of hyperprolactinaemia on the hypothalamo-pituitary axis was assessed by iv injection of 100 μg luteinizing hormone releasing hormone (LRH) in 7 women with prolactinoma before and 3 months after normalization of the Prl level by transsphenoidal surgery. A dose of 20 mg of conjugated oestrogen (Premarin®) was also injected iv into patients with prolactinoma before and 4 months after surgery, and the serum LH levels were determined serially for 120 h after the injection. Surgical treatment caused significant reduction of the mean (± se) serum prolactin (Prl) level from 123.3 ± 7.8 to 19.4 ± 5.6 ng/ml. But the differences in the basal levels of LH (11.3 ± 2.2 to 8.6 ± 1.5 mIU/ml), FSH (8.3 ± 2.4 to 10.6 ± 3.7 mIU/ml) and oestradiol (26.6 ± 8.6 to 37.5 ± 5.5 pg/ml) before and 4 months after surgery were not significant. An exaggerated LH response to LRH in untreated prolactinoma patients was also observed after surgical treatment. After surgical treatment, patients showed LH release with a peak between 48 and 72 h after the injection of Premarin, whereas before treatment they did not show any LH discharge. The mean percent increase in LH between 48 and 72 h was also significantly higher after operation than before operation. These results suggest that the hyperprolactinaemia in prolactinoma patients may cause an impaired positive feedback effect of oestrogen on LH release and that this derangement can be reversed by reduction of the Prl level by adenomectomy.

Abstract. The effect of prostaglandin D₂ on the release of luteinizing hormone was studied in a superfusion system by superfusing human pituitary gland. Perfusion with 30 μg of prostaglandin D₂ induced a significant increase of luteinizing hormone secretion. This is the first evidence of a direct effect of prostaglandin D₂ on the secretion of luteinizing hormone from the human pituitary gland. This finding suggests the possible role of prostaglandin D₂ in human reproductive function

Abstract. The effects of vasoactive intestinal peptide (VIP) on the releases of LH and GnRH were examined in a sequential double chamber perifusion system by perifusing the medio-basal hypothalamus and/or pituitary excised from normal female rats in diestrus or ovariectomized rats. When the medio-basal hypothalamus and pituitary from normal rats in series were perifused with VIP (10⁻⁶ mol/l), the concentration of LH in the efflux was increased by 59–181% above that before the injection (P < 0.05), VIP having a dosedependent effect. VIP had no effect on LH release from the pituitary perifused alone. Infusion of VIP at 10⁻⁶ mol/l induced a significant release (84–159% increase, P < 0.05) of GnRH from the medio-basal hypothalamus. Infusion of 10⁻⁶ mol/l VIP induced a significant release (41–99% increase, P < 0.05) of LH in ovariectomized rats. These findings suggest that VIP induces GnRH release from the medio-basal hypothalamus, resulting in LH release from the pituitary, and that this process does not require ovarian estrogen.

Abstract

The abilities of recombinant human interleukin 1 (IL-1) and IL-6 to induce release of FSH, LH and PRL from rat pituitary cells in vitro were examined. IL-1 and IL-6 induced significant releases of FSH, LH and PRL within 3 h. The extents of release of these compounds induced by IL-1 and IL-6 were similar to those induced by GnRH and TRH. Rat anterior pituitary cells released IL-6 spontaneously, and its release was enhanced by IL-1β. This effect of IL-1β was inhibited significantly by a rabbit anti-IL-1β antiserum. These findings suggest that IL-1 induced the release of IL-6 from rat pituitary, and that the released IL-6 stimulated the secretions of FSH, LH and PRL.

ABSTRACT

In order to define the abnormality in gonadotrophin secretion in Japanese women with polycystic ovaries (PCO) who rarely show virilization and markedly enlarged ovaries, basal levels of LH and FSH, and responses of serum gonadotrophins to LH-releasing hormone (LH-RH) or oestrogens were determined by radioimmunoassay. Eleven patients with PCO diagnosed by laparotomy or laparoscopy and 30 normal women in the follicular phase were studied.

The mean (± sd) basal level of LH was significantly higher in patients with PCO than in normal controls (PCO 28.6 ± 2.4 vs. normal 10.9 ± 3.0 mIU/ml), while the mean FSH level in PCO patients was not significantly different from that in the normal controls (9.7 ± 0.7 vs. 11.4 ± 2.6 mIU/ml). The mean LH/FSH ratio in PCO patients was significantly higher than that in normal controls (3.2 ± 0.9 vs. 1.0 ± 0.3). Exaggerated response of LH to LH-RH was observed in PCO patients, while the FSH response was comparable with the normal controls. Ten out of 11 patients with PCO showed LH release exceeding the basal level after bolus iv injection of 20 mg conjugated oestrogens (Premarin®), and virtually the same mean net increase in LH from the basal level was obtained in both PCO patients and normal controls.

Since the abnormalities in gonadotrophin secretion in Japanese women with PCO are not different from those reported in patients with PCO in Europe and USA, it seems likely that lower incidence of markedly enlarged ovaries and virilization in Japanese patients may be caused by the difference in ovarian response to gonadotrophin.