日本内分泌学会雑誌
Online ISSN : 2186-506X
Print ISSN : 0029-0661
ISSN-L : 0029-0661
67 巻, 5 号
選択された号の論文の7件中1~7を表示しています
  • 布施 秀樹, 水野 一郎, 片山 喬, 栗本 文彦, 堀内 淳子
    1991 年 67 巻 5 号 p. 587-596
    発行日: 1991/05/20
    公開日: 2012/09/24
    ジャーナル フリー
    Epidermal growth factor (EGF), a polypeptide hormone originally discovered in the mouse submaxillary gland, stimulates growth in a variety of tissues in several species. This hormone has recently been identified in human urine. Herein, radioimmunoassay (RIA) for human EGF (hEGF) has been developed, using human recombinant EGF as reference standard and radioiodinated tracer and antibodies raised against hEGF. Its sensitivity was somewhat higher than that of RIAs reported formerly. This method had no cross reactivity with high molecular weight EGF. Urinary concentrations of hEGF in normal males and females were 30.2±13.0ng/mg creatinine and 46.4±17.4ng/mg creatinine, respectively. Urinary concentration of hEGF in patients with renal cancer was somewhat low. The patients with bladder cancer had lower urinary excretion of hEGF than normal adults (p<0.05). However, the role of hEGF in health and disease remains to be determined.
  • 下垂体小人症との比較
    田中 敏章, 日比 逸郎, 鎮目 和夫
    1991 年 67 巻 5 号 p. 597-610
    発行日: 1991/05/20
    公開日: 2012/09/24
    ジャーナル フリー
    The relations of GH secretion capacity by stimulation tests to clinical characteristics and the effect of GH treatment were studied in 151 girls with Turner syndrome and were compared with those in 128 patients with pituitary dwarfism.
    GH secretion capacity expressed by mean peak GH was not associated with clinical characteristics related to growth such as height SDS and growth velocity SDS in Turner syndrome and was influenced by % overweight, whereas it was associated with growth-related clinical characteristics in pituitary dwarfism. Because GH secretion capacity does not affect growth in Turner syndrome, it is not reasonable to diagnose low peak GH in stimulation tests as GH deficiency in Turner syndrome.
    GH treatment increased the growth velocity and growth velocity SD score in Turner syndrome in a dose-dependent manner. In pituitary dwarfism, the effect of GH treatment expressed by the increase in growth velocity SD score had a negative correlation with growth velocity SD score before GH treatment and GH secretion capacity, which indicated that GH treatment was replacement therapy. In Turner syndrome, the effect of GH treatment had a negative correlation with growth velocity and growth velocity SD score before GH treatment, but had no relation to GH secretion capacity, which suggested that GH treatment did not provide replacement GH but had another pharmacological effect.
  • 城田 俊英
    1991 年 67 巻 5 号 p. 611-621
    発行日: 1991/05/20
    公開日: 2012/09/24
    ジャーナル フリー
    To delineate the pathophysiological basis for increased blood urea nitrogen (BUN), decreased serum creatinine (SCr) and increased BUN/SCr ratio in patients with hyperthyroidism due to Graves' disease, systematic evaluation on renal handling of solutes and water was carried out before and during treatment of the disease.
    First, BUN, SCr, serum sodium (Na), serum potassium (K), serum chloride (Cl), creatine kinase (CK), serum triiodothyronine (T3) and serum thyroxine (T4) were consecutively measured in 16 patients (aged 18-62 yrs, 4 males and 12 females) with Graves' disease before and during antithyroid drug therapy, and 16 healthy subjects (aged 22-64 yrs, 4 males and 12 females) served as controls.
    BUN (14.8±2.9mg/100ml) was significantly higher (p<0.01), and SCr (0.62±0.16mg/100ml) and CK (41.7±23.6U/l) were significantly lower (p<0.01) in untreated patients compared to respective values in the control group (BUN, 13.2±2.9mg/100ml; SCr, 0.87±0.16mg/100ml; CK, 99.3±49.5U/l). Consequently, BUN/SCr ratio was significantly elevated (p<0.01) in the patients. As T4 and T3 returned to normal, BUN, SCr, BUN/SCr ratio and CK of the patients also normalized. Serum electrolytes were not significantly different in the patients compared to the controls.
    Second, renal clearance of para-aminohippurate (CPAH), inulin (CIN), creatinine (CCr), free water (CH2O) and chloride (CCl) was evaluated in 7 untreated patients (aged 17-44 yrs, 4 males and 3 females) and in 7 controls (aged 24-39 yrs, 5 males and 2 females).
    In patients with untreated Graves' disease, CPAH/CCr and Curea. were significantly greater than in the controls (847±367 vs 442±124ml/min, p<0.05, 132.7±14.7 vs 76.6±14.4ml/min, p<0.01, and 86.9±16.0ml/min vs 52.1±12.6ml/min, p<0.05, respectively). CIn. was slightly but insignificantly increased in the patients (95.3±20.8ml/min) compared to the controls (76.7±13.3ml/min). As a result, CCr/CIn and Curea/CIn were significantly greater in the patients than in the controls (142.7±32.0 vs 100.7±7.1%, p<0.01, 92.4±18.7 vs 68.4±14.4%, p<0.05, respectively). The difference between CCr and CIn indicates that 40% of urinary creatinine is of tubular origin. Renal excretion of urea and creatinine was increased by 117% and decreased by 77%, respectively in the patients, but the differences were not statistically significant. Distal tubule delivery{DTD, (CH2O+CCl)/CIn×100}in the patients was significantly less than in the controls (6.76±4.60 vs 13.1±2.7%, p<0.05), but distal fractional chloride reabsorption{DFCR, CH2O/(CH2O+CCl)×100}was not significantly different.
    We conclude that in patients with Graves' disease, 1) BUN/SCr ratio is increased due to elevation of BUN and decrease of SCr, 2) elevation of BUN is due to increased urea production but not due to decreased urinary excretion, 3) decreased serum creatinine is due to increased renal clearance resulting from excessive tubular secretion, and decreased creatinine production may also contribute to low SCr, 4) distal tubule delivery is decreased, suggesting an increase in reabsorption of water and sodium from the proximal tubule and/or the loop of Henle.
  • 大豆投与実験
    石突 吉持, 広岡 良文, 村田 善晴, 富樫 和美
    1991 年 67 巻 5 号 p. 622-629
    発行日: 1991/05/20
    公開日: 2012/09/24
    ジャーナル フリー
    To elucidate whether soybeans would suppress the thyroid function in healthy adults, we selected 37 subjects who had never had goiters or serum antithyroid antibodies. They were given 30g of soybeans everyday and were divided into 3 groups subject to age and duration of soybean administration.
    In group 1, 20 subjects were given soybeans for 1 month. Groups 2 and 3 were composed of 7 younger subjects (mean 29 y. o.) and 10 elder subjects (mean 61 y. o.) respectively, and the subjects belonging to these groups received soybeans for 3 months. The Wilcoxon-test and t-test were used in the statistical analyses. In all groups, the various parameters of serum thyroid hormones remained unchanged by taking soybeans, however TSH levels rose significantly although they stayed within normal ranges. The TSH response after TRH stimulation in group 3 revealed a more significant increase than that ingroup 2, although inorganic iodide levels were lowered during the administration of the soybeans. We have not obtained any significant correlation between serum inorganic iodide and TSH.
    Hypometabolic symptoms (malaise, constipation, sleepiness) and goiters appeared in half the subjects in groups 2 and 3 after taking soybeans for 3 months, but they disappeared 1 month after the cessation of soybean ingestion.
    These findings suggested that excessive soybean ingestion for a certain duration might suppress thyroid function and cause goiters in healthy people, especially elderly subjects.
  • 瀬戸口 純子, 中埜 幸治, 〓 義信, 青木 眞一郎, 沢田 学, 長谷川 剛二, 金綱 隆弘, 近藤 元治
    1991 年 67 巻 5 号 p. 630-635
    発行日: 1991/05/20
    公開日: 2012/09/24
    ジャーナル フリー
    To investigate the immunological process in various thyroid disease, we measured interferon-alpha, -gamma (IFN-α,-γ), natural killer (NK) activity, and lymphocyte subsets in the peripheral blood of 27 patients with Basedow's disease (BD) (M: F=9: 18), 8 with Hashimoto's thyroiditis (HT) (2: 6), 5 with idiopathic hypothyroidism (IHT) (1: 4), and normal controls (C).
    IFN-α, -γ levels were measured by bioassay with Dye-uptake method, and NK activity was measured by the LDH method. The mean_??_SD levels of IFN-γ in BD, HT, IHT, and C (N=217) were 173.9±88.0, 288.0±134.9, 120.4±38.0 and 173.9±88.0IU/ml, respectively. The IFN-γ level was higher in HT (p<0.05) than in controls, and lower in BD (p<0.02). Moreover, this IFN-γ level did not correspond with the titers of thyroid hormones; TSH, anti-microsome antibody, and anti-TSH-receptor antibody in peripheral blood. However, IFN-α levels and NK activity in the patients of every group were similar to those in controls. The ratios of lymphocyte subsets of peripheral blood were measured by cytofluorometry with monoclonal antibodies. The mean±SD levels of T cells in BD, HT, IHT and C were 75.9±7.0, 83.4±7.2, 85.2±5.7, 82.3±5.8%, and those of B cells were 17.5±6.1, 10.9±4.2, 8.0±5.8, 10.9±5.0%, respectively. The ratio of T cells was higher in IHT (p<0.05) and lower in BD (p<0.01) than in controls. However, the ratio of B cells was lower in IHT (p<0.05), and higher in BD (p<0.01).
    Now it has been reported that the local IFN-γ plays an important role in the onset, maintenance and development of BD. In this study, the peripheral IFN-γ level in BD was low despite high levels in the thyroid gland. We speculate these paradoxical IFN-γ levels are related to auto-regulation of cytokines, or T lymphocyte impairment in autoimmune thyroid diseases.
  • 安達 知子, 岩下 光利, 渡辺 正子, 武田 佳彦, 坂元 正一
    1991 年 67 巻 5 号 p. 636-644
    発行日: 1991/05/20
    公開日: 2012/09/24
    ジャーナル フリー
    Insulin-like growth factor-I (IGF-I) is a polypeptide that mediates growth-promoting actions of GH and has insulin-like activity. Increase in the levels of IGF-I in the maternal and fetal circulation during pregnancy and the identification of the specific receptors for IGF-I in a variety of fetal tissues suggest that IGF-I may play a significant role in the regulation of fetal growth. The present study was undertaken to determine the significance of maternal IGF-I on fetal and placental growth by administering the specific antiserum for IGF-I to pregnant mice. The antiserum was produced by repeatedly injecting recombinant IGF-I into rabbits. The antiserum obtained showed 30% binding to 125I-IGF-I at a dilution of 1: 240,000, and crossreactivity with IGF-II was 0.012%. In the first set of experiments, pregnant mice were given a daily dose of 50μl of the original antiserum (E-1) or normal rabbit serum (C-1) into the peritoneal cavity between Day 3 and 10. In the second set of experiments, antiserum (E-2) or normal rabbit serum (C-2) was administered between Day 11 and 18. On Day 18, all mice were killed, blood was collected for measurement of levels of IGF-I by RIA, and the weights of fetuses and placentas in individual mice were recorded. The maternal levels of IGF-I in group E-1 and E-2 were extremely low compared to those in group C-1 and C-2. The number of fetuses and rate of abortion among each group were not significant. However, the average weight of fetus in group E-1 (1235.1±16.2mg, mean±SE, n=32) and E-2 (1298.6±15.0mg, n=38) was significantly lower (p<0.001) than that in C-1 (1470.6±12.7mg, n=35) and C-2 (1360.5±12.7mg, n=26). Similarly, the average weight of placenta in group E-1 (71.6±2.1mg) and E-2 (74.5±2.6mg) was lower (p<0.001) than that in C-1 (101.9±1.9mg) and C-2 (105.7±4.0mg). These results indicate that IGF-I in the maternal circulation has an important role in regulating fetal and placental development.
  • 湯浅 久子, 鈴木 孝憲, 今井 強一, 山中 英寿, 神野 英毅
    1991 年 67 巻 5 号 p. 645-654
    発行日: 1991/05/20
    公開日: 2012/09/24
    ジャーナル フリー
    In this study, we investigated the dependency of estramustine binding protein (EMBP) from rat prostate on endogeneous androgen. The EMBP content of the dorsolateral prostate markedly decreased 14 days after castration and increased again after the cessation of the weekly subcutaneous administration of 2 mg of Estradio1-17β valerate, in accordance with the recovery of prostate weight and serum testosterone concentration. This result clearly demonstrated that EMBP, which was present in very small quantities in the dorsolateral prostate, had a dependency on endogeneous androgen as well as on the ventral prostate EMBP. We investigated the changes in prostate weights, EMBP concentration and serum testosterone level throughout life. The ventral prostate weight began to increase rapidly at 7 weeks of age and showed a broad peak from 11 to 14 weeks of age and then gradually decreased. On the other hand, the dorsolateral prostate weight began to increase rapidly at 7 weeks of age and continued to increase very gradually even after 10 weeks of age. There was a remarkable difference in the changes in EMBP concentration between the ventral prostate and the dorsolateral prostate.
    In the ventral prostate, EMBP concentration increased markedly from 4 to 9 weeks of age. Thereafter it continued to increase very gradually. On the other hand, in the case of the dorsolateral prostate, EMBP demonstrated higher and fluctuating concentration from 4 to 15 weeks of age. After 16 weeks of age, EMBP showed lower and stable concentration, although the weight of dorsolateral prostate showed gradual increase. These results suggested that there exist, beside androgens, some factors that participated in the regulation of growth and functional metabolism in the dorsolateral prostate after 16 weeks of age.
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