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ABSTRACT
To clarify the mechanism(s) underlying the TRH-induced refractory state of the anterior pituitary, we evaluated rat pituitary inositol phospholipid hydrolysis in the presence of staurosporine. TRH caused a time- and dose-dependent accumulation of inositol phosphates in rat anterior pituitary slices. Pretreatment with 550 nmol TRH/l completely abolished the subsequent accumulation of inositol phosphates in response to 140 nmol TRH/l. TRH-stimulated accumulation of inositol phosphates did not occur after pretreatment with 0·2 μmol phorbol ester/l. Refractoriness of inositol phospholipid hydrolysis which was produced by pretreatment with TRH and phorbol ester was inhibited by staurosporine. The present data support the hypothesis that protein kinase C plays a profound role in TRH induction of the refractory state of inositol phospholipid hydrolysis in the anterior pituitary.
Journal of Endocrinology (1990) 124, 75–79
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Department of Obstetrics and Gynecology, Kyoto University School of Medicine, Sakyo-ku, Kyoto and * Division of Pharmacology, Teikoku Hormone Research Institute, Kawasaki, Japan
(Received 1 October 1976)
It is well known that ovulation is brought about by a surge of luteinizing hormone (LH). Ovarian steroidogenesis induced by LH has been implicated in the ovulatory process by the observation that ovulation is prevented by various inhibitors of steroidogenesis in immature rats primed with pregnant mare serum gonadotrophin (PMSG) (Lipner & Greep, 1971). Subsequently doubt was cast on this concept (Bullock & Kappauf, 1973), but recently it has been reported that a progesterone-dependent step exists in the normal ovulatory process in cyclic rats (Takahashi, Ford, Yoshinaga & Greep, 1974). However, the involvement of oestrogen in follicular rupture was not excluded in any of these experiments. In an attempt to obtain direct evidence of whether either steroid and, if so which, is essential for
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SUMMARY
Neonatal treatment of female mice with oestrogen or androgen induces persistent vaginal cornification, which may be dependent or independent of ovarian hormones according to the amount administered. The concentration of oestrogen-binding protein in the cytoplasm and in the nuclear fraction was measured in the uterus and vagina of mice treated neonatally with either steroid alone or in combination with prolactin. Vaginal oestrogen responsiveness (dependence) of mice treated with low and high doses of steroids was correlated with oestrogen receptor content. Neonatal treatment with prolactin in combination with the low dosage steroid treatments favoured development of ovary-independent cornification and a concomitant decrease in oestrogen receptors in about 50% of the mice studied.
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SUMMARY
A 27-year-old patient with a hilus cell tumour of the ovary giving rise to secondary amenorrhea and marked virilization was studied clinically and endocrinologically, and the tumour was examined by light and electron microscopy. Clinical, roentogenological and endocrinological studies showed that the ovarian tumour was the source of excessive androgen production. Urinary 17-oxosteroid excretion was always higher than 65 mg./day. The urinary production rates of testosterone, dehydroepiandrosterone and dehydroepiandrosterone sulphate were 1970 mg./day, 98·5 mg./day and 31·9 mg./day, respectively. Postoperatively, the androgenic manifestations gradually subsided, and the menstrual cycle returned to normal.
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ABSTRACT
Plasminogen activator (PA) activity in the rat uterus was measured at fixed intervals post partum in order to determine whether this serine protease increases during the acute remodelling of tissue which occurs in the involuting uterus. Plasminogen activator activity was measured by an indirect method based on the hydrolysis of the chromogenic substrate S-2251 by PA-generated plasmin. At the time of parturition the control level of PA activity was 0·033 ± 0·018 (s.d.) μmol/4 mg uterine wet weight per 30 min. This activity increased fourfold to a peak of 0·131 ±0·036 at 3 days post partum, and then it declined steadily towards the control level during the next 7 days. Concomitantly, uterine weight decreased to 25% of the control weight by 3 days post partum, and it continued to decrease until day 15. In the 30 days post partum during which PA activity was monitored there was no significant change in plasmin inhibitors in the uterine extracts. The results suggest a correlation between PA activity and the process of tissue remodelling which occurs during involution of the rat uterus. This increase in PA might serve to activate a latent collagenase since the measured peak in PA activity happens to coincide with a reported increase in collagenolytic activity in the involuting rat uterus.
J. Endocr. (1985) 104, 295–298
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The thyromimetic compound SK&F L-94901 shows more potent thyromimetic activity in the liver than in the pituitary gland or heart when administered to rats. The mechanisms of liver-selectivity of SK&F L-94901 were examined using cultured rat hepatoma cells (dRLH-84) and rat pituitary tumor cells (GH3), both of which showed saturable cellular uptake of tri-iodothyronine (T(3)). When isolated nuclei with partial disruption of the outer nuclear membrane were used, SK L-94901 competed for [(125)I]T(3) binding to nuclear receptors almost equally in dRLH-84 and GH3 cells. SK L-94901 also did not discriminate thyroid hormone receptors (TR) alpha1 and beta1 in terms of binding affinity and activation of the thyroid hormone responsive element. In intact cells, however, SK L-94901 was a more potent inhibitor of nuclear [(125)I]T(3) binding in dRLH-84 cells than in GH3 cells at an early phase of the nuclear uptake process and after binding equilibrium. These data suggest that SK L-94901 is more effectively transported to nuclear TRs in hepatic cells than in pituitary cells and therefore shows liver-selective thyromimetic activity. In conclusion, SK L-94901 discriminates hepatic cells and pituitary cells at the nuclear transport process. The cellular transporters responsible for this discrimination were not evident.
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Abstract
The decrease in estrogen in menopausal women increases body fat. The present studies were undertaken to investigate the involvement of estrogen in leptin production in vivo. In the first study, expression of ob gene mRNA in white adipose tissue was measured at 2 and 8 weeks after ovariectomy in rats. In the second, serum leptin concentration was measured in total body fat of 87 weight-matched human subjects (29 men, 29 premenopausal and 29 postmenopausal women). In the third, changes in serum leptin concentration with the menstrual cycle were determined, ob gene expression decreased in subcutaneous and retroperitoneal white adipose tissue of ovariectomized rats 8 weeks after the operation, while ovariectomy increased ob gene expression in mesenteric white adipose tissue. Serum leptin concentration was decreased by ovariectomy. Estradiol supplement reversed the effect of ovariectomy on ob gene expression and circulating leptin levels. In humans, serum leptin concentration was higher in premenopausal women than in men, and in postmenopausal women it was lower than in premenopausal women, but still higher than in men. In 13 premenopausal women, serum leptin levels were significantly higher in the luteal phase than in the follicular phase. The present studies strongly indicate that estrogen regulates leptin production in rats and human subjects in vivo. Regional variation in the regulation of ob gene expression by estrogen was found.
Journal of Endocrinology (1997) 154, 285–292
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ABSTRACT
An influence of thyrotrophin-releasing hormone (TRH) on TSH heterogeneity in close association with de-novo biosynthesis was studied in rat anterior pituitary glands. Hemipituitary glands from adult male rats were incubated in Krebs–Henseleit–glucose media containing [3H]glucosamine and [14C]alanine for 3 and 6 h in the presence or absence of 10 ng TRH per ml. Fractions of TSH in the pituitary extracts were obtained using affinity chromatography coupled with an anti-rat TSH globulin. These TSH fractions were analysed by isoelectric focusing. The control pituitary glands were composed of four component peaks (isoelectric point (pI) 8·7, 7·8, 5·3 and 2·5) of [3H]glucosamine and [14C]alanine incorporated into TSH, and the amounts of radioactivity of these components were increased with the incubation time. Of these peaks, radioactive components of pI 8·7 and 7·8 coincided with the non-radioactive TSH components measured by radioimmunoassay. Addition of TRH increased incorporation of [14C]alanine into TSH in each of the components to a greater extent than that of [3H]glucosamine. In addition, new components with pI 7·2, 6·5 and 6·2, each component corresponding to each unlabelled TSH component, were demonstrated in the presence of TRH. Because addition of TRH did not change the amounts of [14C]alanine-labelled TSH in the media, the newly formed components were assumed to be connected with protein synthesis occurring in the anterior pituitary gland, which may be specific substances in response to TRH administration. These results indicate that TRH principally elicits an increase in protein synthesis in TSH at the anterior pituitary level, resulting in an alteration of TSH heterogeneity.
J. Endocr. (1984) 103, 165–171
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Abstract
The plasma concentration and liver mRNA content of IGF-I are regulated by the quantity and quality of dietary proteins. To determine whether the synthesis of IGF-binding proteins (BPs) is also affected by protein nutrition, we assessed plasma concentration, tissue mRNA content and liver transcription rate of each BP after rats were fed either a 12% casein or a protein-free diet for 1 week. Protein deprivation reduced the plasma concentration of IGFBP-3 and IGFBP-4 and increased that of IGFBP-1 and IGFBP-2. The mRNA content in tissues and liver transcription rates of IGFBP-3 and IGFBP-4 did not change in response to protein deprivation although their plasma concentrations decreased. The increased plasma IGFBP-1 and IGFBP-2 concentrations were explained by the increased mRNA content and transcription rate of their genes in the liver. Although IGFBP-1 mRNA was increased by protein deprivation not only in liver but also in kidney, IGFBP-2 mRNA was increased only in liver and did not increase in any other tissue examined. In addition, the liver mRNA content of the acid-labile subunit, which can form a ternary complex with IGFs and IGFBP-3, was not affected by protein deprivation. These results show that tissue-specific synthesis of each BP is regulated in a distinct way in response to protein deprivation.
Journal of Endocrinology (1996) 150, 33–41
Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Department of Anatomy, Showa University School of Medicine, Tokyo 142-8555, Japan
Discovery Research Laboratories, Pharmaceuticals Research Division, Takeda Chemical Industries, Ibaraki 300-4293, Japan
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Neuropeptide W (NPW) is a 30-amino-acid peptide initially isolated from the porcine hypothalamus as an endogenous ligand for the G protein-coupled receptors GPR7 and GPR8. An intracerebroventricular administration of NPW increased serum prolactin and corticosterone concentrations, decreased dark-phase feeding, raised energy expenditure, and lowered body weight. Peripherally, GPR7 receptors are abundantly expressed throughout the gastrointestinal tract; the presence of NPW in the gastrointestinal endocrine system, however, remains unstudied. Using monoclonal and polyclonal antibodies raised against rat NPW, we studied the localization of NPW in the rat, mouse, and human stomach by light and electron microscopy. NPW-immunoreactive cells were identified within the gastric antral glands in all three species. Double immunohistochemistry and electron-microscopic immunohistochemistry studies in rats demonstrated that NPW is present in antral gastrin (G) cells. NPW immunoreactivity localized to round, intermediate-to-high-density granules in G cells. NPW-immunoreactive cells accounted for 90% chromagranin A- and 85% gastrin-immunoreactive endocrine cells in the rat gastric antral glands. Using reversed-phase HPLC coupled with enzyme immunoassays specific for NPW, we detected NPW30 and its C-terminally truncated form, NPW23, in the gastric mucosa. Plasma NPW concentration of the gastric antrum was significantly higher than that of the systemic vein, suggesting that circulating NPW is derived from the stomach. Plasma NPW concentration of the gastric antrum decreased significantly after 15-h fast and increased after refeeding. This is the first report to clarify the presence of NPW peptide in the stomachs of rats, mice, and humans. In conclusion, NPW is produced in gastric antral G cells; our findings will provide clues to additional mechanisms of the regulation of gastric function by this novel brain/gut peptide.
