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64 巻, 10 号
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松本 俊夫, 尾形 悦郎, 孫 孝義, 古川 洋太郎, 岡本 純明, 長瀧 重信, 山根 良太, 竹沢 順一, 飯島 隆1988 年 64 巻 10 号 p. 1015-1023
発行日: 1988/10/20
公開日: 2012/09/24
ジャーナル フリーIn order to evaluate the validity of the direct radioimmunoassay of plasma cAMP level by using Yamasa cyclic AMP assay kit, we determined the cyclic AMP concentration of normal human plasma before and after purification through anion-exchange chromatography. We found that 1) the direct assay before purification gave almost the same values as the indirect assay after purification by anion-exchange chromatography, 2) hemolysis did not affect the results of the direct assay, 3) the plasma cAMP was stable for up to 12 weeks when 5 mM EDTA was added to the blood at the time of sampling and stored below -20°C and 4) the cAMP concentration did not decrease by repeated freeze-thawing of the plasma samples for up to 10 times. These results indicate that the direct radioimmunoassay of plasma cAMP concentration in normal subjects can give the same values as those obtained after purification by anion-exchange chromatography. Although further investigation is needed to clarify whether these results can be equally applied to patient's plasma with various diseases, the direct assay offers a convenient and accurate method to determine plasma cAMP concentration.抄録全体を表示PDF形式でダウンロード (683K) -
特にステロイド生合成機構への関与を中心として高木 耕一郎1988 年 64 巻 10 号 p. 1024-1037
発行日: 1988/10/20
公開日: 2012/09/24
ジャーナル フリーActivities of the steroidogenic enzymes involved in functional luteolysis and PGF2α induced luteolysis were determined in PMSG-hCG primed immature rats to elucidate the luteolytic effects of PGF2α. Plasma progesterone (P4), plasma 20α dihydroprogesterone (20αOHP4), in vitro production of pregnenolone (P5) from endogenous cholesterol in ovarian mitochondria (8,000×g pellet; Mt), activities of 3β hydroxysteroid dehydrogenase (313HSD) in ovarian microsome (105,000×g pellet; Ms) and 20α hydroxysteroid dehydrogenase (20αHSD) in ovarian cytosol (105,000×g supernatant; Sup) were determined. For the investigation of intramitochondrial transport of cholesterol, measurement of free cholesterol (FCh) of Mt and the Lineweaver-Burk plotting for cholesterol side-chain cleavage enzyme (CSCC), prepared by osmotic shock and sonication of Mt, were carried out. Functional life span of the rat corpus luteum was estimated as 12 days post hCG treatment from plasma P4. As plasma P4 decreased, concomitant increase in plasma 20αOHP4 was observed. In vitro production of P5 in Mt correlated well with plasma P4 levels, indicating cholesterol side-chain cleavage reaction is the rate limiting step involved in ovarian steroidogenesis. In contrast, both values of Km and Vmax of CSCC did not change between day 7, on which the highest value of plasma P4 observed, and day 12, on which functional luteolysis was ascertained from plasma P4. Both FCh of Mt and the activity of 3βHSD in Ms remained unchanged during the functional life of the corpus luteum. The activity of 20αHSD in Sup increased from day 10 post hCG treatment in accordance with plasma 20αOHP4. These results indicate that 1) decrease in availability of FCh to CSCC within mitochondria and 2) increase in catabolism of P4 into inactive progestin, 20αOHP4, may play key roles in the functional luteolysis. To compare the events observed in functional luteolysis with PGF2α induced luteolysis, the animals were treated either with PGF2α (1 mg/rat; s.c.), cycloheximide (5 mg/rat; i.p.; CX), or vehicle on day 7 post hCG treatment, and sacrified 1 hour later for the analyses mentioned above. Both plasma P4 and in vitro production of Ps in Mt decreased significantly with PGF2a or CX treatment, whereas the FCh of Mt and the activity of CSCC remained unchanged with PGF2α treatment. Both plasma 20αOHP4 and 20αHSD in Sup increased with PGF2α treatment. However, CX suppressed both of them. These results seem to fit with the findings observed in the functional luteolysis, and therefore, it is suggested that PGF2α might be involved in luteolysis through the blockade of intramitochondrial cholesterol transport and the facilitation of catabolism of P4 into 20αOHP4.抄録全体を表示PDF形式でダウンロード (1524K) -
原 秀雄, 伴 良雄, 佐藤 龍次, 九島 健二, 長倉 穂積, 海原 正宏, 寺本 明1988 年 64 巻 10 号 p. 1038-1050
発行日: 1988/10/20
公開日: 2012/09/24
ジャーナル フリーWe studied the secretion capacity of TSH-β in 63 patients with various pituitary disorders, carrying out the observation of TSH-β changes after TRH administration. Serum TSH-β concentrations were measured by radioimmunoassay according to the modified method of Kourides. Serum TSH concentrations were measured by immunoradiometric assay, and serum concentrations of free thyroid hormones were measured by radioimmunoassay.
Basal TSH-β concentrations were below 0.39 ng/ml in 17 patients with Acromegaly, below 0.56 ng/ml in 5 patients with Prolactinoma, below 0.68 ng/ml in 4 patients with Cushing's disease, below 0.48 ng/ml in 12 patients with non-functioning tumor, below 6.4 ng/ml in 16 patients with SITSH, and below 0.45 ng/ml in 9 patients with other pituitary diseases.
TSH-β changes after TRH administration differed from TSH changes in 4 patients (25%) with Acromegaly, in 2 patients (67%) with Prolactinoma, in 5 patients (71%) with non-functioning tumor, in one patient (33%) with Cushing's disease, in 4 patients (100%) with Rathke's cleft cyst, in one patient with suprasellar meningioma, and in one patient with suprasellar arachinoid cyst.
2 patients (67%) with Prolactinoma, 3 patients (43%) with non-functioning tumor, all 6 patients with non-neoplastic SITSH, and one patient with Rathke's cleft cyst showed exaggerated TSH-β changes after TRH administration.
In patients with some pituitary disorders, we thought the secretion and synthesis of TSH and TSH-β differed from that of normal subjects. We concluded that it was necessary to investigate the mechanism of secretion of TSH-β in patients with pituitary disorders.抄録全体を表示PDF形式でダウンロード (1199K) -
的崎 尚1988 年 64 巻 10 号 p. 1051-1064
発行日: 1988/10/20
公開日: 2012/09/24
ジャーナル フリーTo clarify the possible role of a guanine nucleotide regulatory protein in the signal transducing system activated by cholecystokinin (CCK), the actions of CCK on rat pancreatic acini were compared with those of NaF, which is a well-known activator of stimulatory and inhibitory guanine nucleotide regulatory proteins. Guanine nucleotides reduced the binding of 125I-CCK-octapeptide (CCK8) to acinar cell membranes, with the rank order of potency being guanyl-5′-yl imidodiphosphate (Gpp (NH) p) >GTP>GDP>GMP. Scatchard analysis of labeled CCK binding revealed that the decrease in CCK binding caused by Gpp (NH) p was due to the decrease in an affinity constant of CCK for its receptors with no signficant change in the maximal binding capacity.
When acini were incubated with increasing concentrations of either CCK8 or NaF, maximal stimulation of amylase release occurred at 100 pM CCK8 or 10 mM NaF, respectively, and supramaximal concentrations of CCK8 or NaF caused its submaximal stimulation. Further, CCK and NaF similarly stimulated the hydrolysis of polyphosphoinositide in acini and the release of Ca2+ from the intracellular Ca2+ store into the cytoplasm although there was a lag period prior to any detectable stimulation by NaF. The doses of NaF necessary for Ca2+ mobilization and inositol phosphate generation were nearly the same, with a maximal stimulation at 20 mM NaF. NaF, at concentrations up to 20 mM, a supramaximal concentration for amylase release, produced no significant change in the cellular cyclic AMP level. In addition, 10 mM NaF potentiated the amylase release stimulated by VIP, a wellknown secretagogue which functions via cyclic AMP, suggesting that the stimulatory effects of NaF are independent of cellular cyclic AMP.
Gpp (NH) p also activated the hydrolysis of polyphosphoinositide in a cell-free pancreatic acinar cell membrane preparation, with a half-maximal and a maximal stimulation at 1 μM and 10μM, respectively. Furthermore, the effects of submaximal concentrations of CCK8 on polyphosphoinositide hydrolysis were markedly potentiated in the presence of 100 μM GTP, which alone was ineffective.
These results, therefore, strongly suggest that pancreatic CCK receptors may be coupled to the activation of polyphosphoinositide breakdown by a guanine nucleotide regulatory protein.抄録全体を表示PDF形式でダウンロード (1410K) -
赤井 裕輝1988 年 64 巻 10 号 p. 1065-1080
発行日: 1988/10/20
公開日: 2012/09/24
ジャーナル フリーBig gastrin comprising 34 amino acid residues (G34) consists of an N-terminal pentadecapeptide linked via two lysine residues to a C-terminal heptadecapeptide identical with little gastrin (G17). Both G17 and G34 have now been established as the principal active forms of gastrin. In this study, release of G34 N-terminal peptide fragment of methacholine and porcine gastrin releasing peptide (pGRP) stimulation in isolated rat stomach perfusion system was investigated by radioimmunoassay with use of an antiserum specific to the N-terminal portion of G34.
G34 N-terminal immunoreactivity (IR-G34-N) was detected in rat stomach and proximal duodenum, and the highest concentration was found in extract of the antral mucosa. The concentration of IR-G34-N was constantly lower than that of IR-G17. By gel-filtration study, IR-G34-N in antral mucosa extract was attributed mostly to the G34 N-terminal pentadecapeptide-like component, and the concentration of G34 was about one tenth of G17.
Methacholine 10-8-10-3M produced a biphasic dose-dependent release of IR-G34-N from the vascularly perfused isolated rat stomach. The maximal release was shown by 10-5M of methacholine. The release was concomitant with that of IR-G17 during methacholine stimulation. Stimulation of pGRP (14-27) (10-7M) produced a monophasic release of IR-G34-N from the vascularly perfused isolated rat stomach. The release was concomitant with that of G17 during the stimulation. The integrated IR-G34-N release was not stoichiometric with that of IR-G17, and IR-G34-N was constantly low. Gel-filtration of the persusate from rat stomach revealed the presence of the G34 N-terminal pentadecapeptidelike component as a sole major component.
The present results demonstrate that post-translational processing of the gastrin precursor in the rat antrum did not necessarily produce G34, which is further converted in the tissue to G17-related peptide (s) and that the G34 N-terminal fragment formed in the G34 conversion is stored and released concomitantly with G17-related peptide (s).抄録全体を表示PDF形式でダウンロード (1483K) -
高橋 徹, 坂元 秀樹, 大谷 香, 鈴木 英夫, 田 根培, 高木 繁夫1988 年 64 巻 10 号 p. 1081-1087
発行日: 1988/10/20
公開日: 2012/09/24
ジャーナル フリーPregnant rats were injected with 3H RU38486 into the uterine cavity on day 2, 4, 5 and 8 of pregnancy. Before implantation, the saturable RU binding increased significantly (day 2 vs. 4; 30.0±2.3 vs. 640.0±17.9 dpm/g, p<0.001). After implantation, the binding became higher at the nidation site (implantation vs. non-implantation site; 1156.1±237.1 vs. 595.0±24.3, p<0.001, day 5). The dexamethasone suppressive RU binding, on the other hand, showed no significant increase during day 4, 5 and 8.
Daily administration of RU38486 during day 4 and 8 caused failure to implant or to develop normal conceptus. The endometrium in these RU treated animals was stained for tissue glycogen and studied light microscopically. The tissue glycogen content appeared to be markedly decreased in RU treated animals but only at the site of implantation. The decrease was observed in both decidua and trophoblasts but not in myometrium or decidual epithels.
The present results indicate;
(1) In rats, endometrial progesterone binding increases prior to implantation.
(2) After implantation, the nidation site further increases its saturable progesterone uptake compared to the non-implantation site.
(3) When normal process of implantation is inhibited by RU38486 administration, there occurs a decrease in the glycogen systhesis at the nidation site, including decidua and trophoblasts.抄録全体を表示PDF形式でダウンロード (1340K) -
木村 孔三, 水上 尚典, 玉田 太朗1988 年 64 巻 10 号 p. 1088-1101
発行日: 1988/10/20
公開日: 2012/09/24
ジャーナル フリーTo study the prognosis of adolescent ovulatory disturbance in patients with persist-ently elevated LH levels (?25mIU/ml), normal FSH levels and high LH/FSH (>2.0), 17 patients aged 12-19 years were studied longitudinally for 4-9 years. These 17 patients consisted of 7 patients suffering from amenorrhea with estrogenic effect, 5 patients with functional bleeding, 3 patients with delayed menarche and 2 patients with oligomenorrhea. All of the patients showed exaggerated LH responses to 100 μg of LHRH administration while the FSH responses were not different from those obtained from normal women. Out of the 17 patients, 10 (58.8%) patients showed the values of testosterone and 7 (41.2%) androstenedione which were above the mean + 2SD of normal women. Consequently, the mean serum testosterone and androstenedione levels were significantly higher than those in normal women. The mean LH (36.6±8.3 mIU/ml), FSH (11.2±1.5 mIU/ml) and LH/FSH (3.3±0.8) at the age of 21.4±2.5 years were not different from the mean LH (39.9±13.3 mIU/ml), FSH (10.8±1.8 mIU/ml) and LH/FSH (3.8±1.5) at the age of 16.1±1.8 years. respectively. None of the 17 patients showed amelioration or deterioration of ovulatory disturbance during long-term observation. To further investigate the central dopamine activity, 10 mg of metoclopramide (MCP) was administered intravenously in these 17 patients. The LH and PRL responses to MCP were evaluated, and the results were compared to those obtained from 17 patients aged over 20 with PCO and from 17 normal women. The LH responses to MCP were positive in this juvenile patient group and the patients aged over 20 PCO group. However, the LH responses to MCP were negative in normal women in both the follicular and luteal phases. In contrast, the PRL responses to MCP were significantly attenuated in juvenile patients and in patients aged over 20 with PCO compared to those in normal women. Since the hormonal profiles in these 17 patients with anovulation or oligoovulation were very similar to those in the group aged over 20 with established PCO, it may be suggested that 1) at least part of the adult patients with PCO may have had PCO from late adolescence; 2) the majority of the patients with high LH and normal FSH levels in adolescence will suffer from ovulatory disturbance continuously; 3) in these patients, an aberration of central dopamine in control of LH and PRL may exist.抄録全体を表示PDF形式でダウンロード (1373K) -
中村 佐栄子, 出村 黎子, 小松 ひろみ, 鈴木 智晴, 地曳 和子, 小田桐 恵美, 出村 博1988 年 64 巻 10 号 p. 1102-1114
発行日: 1988/10/20
公開日: 2012/09/24
ジャーナル フリーTo investigate the significance of changes in ovarian inhibin in gonadal dysfunction with persistent estrus, female rats with persistent estrus were studied as animal model for polycystic ovaries (PCO). Newborn female Wistar rats treated with testosterone propionate s.c. (TP) and female rats raised under continuous light (LL) started at 9 weeks of age entered into continuous estrus 5 and 2 or 3 weeks after the treatment, respectively. Ovaries in both groups had many polycystic follicles Normal adult female rats with 4 day cycles were served as control. Ovarian inhibin content was measured by FSH suppressing activity of charcoaltreated ovarian homogenates using a rat anterior pituitary cell culture system. Blood samples were obtained at 11 : 00 a.m. and plasma levels of LH, FSH, PRL, estradiol (E2), progesterone (P) and testosterone were measured by RIA. Comparisons were made statistically between each experimental group and normal proestrus (PE). Both LH and FSH were similar to normal PE in TP LL, suggesting a lack of LH and FSH surges probably through hypothalamic dysfunction in TP and LL. Plasma PRL levels were variably elevated in both groups. Ovarian inhibin contents were comparably high to PE in both groups with parallel increases in plasma E2 and P. Plasma testosterone was elevated only in TP. In conclusion, female rats with persistent estrus induced by TP or LL exhibited polycystic ovarian changes similar to PCO. Increased inhibin content in TP and LL may reflect persistent follicular activity.抄録全体を表示PDF形式でダウンロード (1276K)
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