日本内分泌学会雑誌
Online ISSN : 2186-506X
Print ISSN : 0029-0661
ISSN-L : 0029-0661
64 巻, 7 号
選択された号の論文の9件中1~9を表示しています
  • 国広 潔, 野口 志郎, 村上 信夫, 加藤 亮二, 織部 安裕, 高木 良三郎
    1988 年 64 巻 7 号 p. 531-538
    発行日: 1988/07/20
    公開日: 2012/09/24
    ジャーナル フリー
    In order to investigate effects of thyroid hormone on ketone bodies metabolism, fasting levels of serum ketone bodies, serum free fatty acids (FFA), serum insulin (IRI), plasma glucagon (IRG) and plasma glucose were examined in 29 untreated patients with hyperthyroidism and 20 healthy subjects. In 21 patients the levels of serum ketone bodies were re-examined when euthyroidism was achieved after treatment. In all of healthy subjects and 17 patients changes in the levels of serum ketone bodies after oral glucose load were examined. The results were as follows.
    1), Fasting levels of serum FFA and total ketone bodies (TK), acetoacetate (AcAc), 3- hydroxy-β-butylate (3OHBA), ratio of 3OHBA to AcAc in the patients were significantly higher than those in healthy subjects. The levels of IRI, IRG or ratio of IRG to IRI in the patients were not different from those in healthy subjects. In the patients, the fasting level of TK was significantly correlated with the level of FFA.
    2), After oral glucose load the levels of TK and FFA in the patients decreased gradually.
    3), The fasting levels of TK and FFA in the patients decreased when euthyroidism was achieved after treatment.
    It was suggested that the fasting levels of serum ketone bodies in patients with hyper-thyroidism elevated probably due to activated lipolysis.
  • (第II報) 腎原性cyclic AMP及び血清副甲状腺ホルモン免疫活性について
    吉田 ひとみ, 木下 眞男, 大島 久二, 斉藤 栄造
    1988 年 64 巻 7 号 p. 539-546
    発行日: 1988/07/20
    公開日: 2012/09/24
    ジャーナル フリー
    Myotonic dystrophy (MyD) is a multisystemic disorder characterized by muscle atrophy, myotonia and cataract. Although a number of reports have been accumulated showing the presence of bone changes in MyD patients, there are few published papers in which calcium metabolism was precisely examined. In the preveious paper, we reported that intestinal calcium absorption was increased in MyD patients due to the elevation of plasma 1, 25 (OH) 2D level. The present study was designed to elucidate the mechanism of increased level of serum 1, 25 (OH) 2 D concentration in MyD patients.
    Calcium tolerance tests were performed in 13 patients with MyD, 13 patients with other neuromuscular disorders (non-MyD) and 12 healthy control subjects according to the method of Broadus et al. Immunoreactive PTH (iPTH) levels and cyclic AMP (cAMP) levels were measured using commercially available RIA kits.
    The basal plasma calcium levels in MyD were slightly higher than those in the other two groups, but the difference was not statistically significant. The plasma 1, 25 (OH) 2 D levels, calcemic responses and calciuric responses in MyD were significantly higher than those in the other two groups. Serum iPTH levels in MyD (0.462±0.320ng/ml, Mean±SD) were significantly higher than those in the other two groups (normal subjects 0.175±0.092, non-MyD 0.200±0.111; p<0.02). Nephrogenous cyclic AMP (NcAMP) levels in MyD (2.094 ±3.244nmol/100mlGF) were also higher than those in normal subjects (0.907±0.212, p< 0.05) and in non-MyD (0.929±0.335, p<0.05). There was a significant correlation between serum iPTH levels and NcAMP levels, and therefore it might be possible to accept that these two measurements reflect the level of parathyroid funciton. There were also significant correlations between NcAMP and plasma 1, 25 (OH) 2D levels, calcemic responses and calciuric responses (p<0.01).
    The present study shows that parathyroid hormone function was augmented in MyD patients. Hence, increased levels of palsma 1, 25 (OH) 2 D shown in MyD is considered to be the result of hyperparathyroid state in these patients.
  • 吉田 ひとみ
    1988 年 64 巻 7 号 p. 547-553
    発行日: 1988/07/20
    公開日: 2012/09/24
    ジャーナル フリー
    Although the presence of bone abnormalities has been well known in myotonic dystrophy (MyD), details about calcium metabolism in this condition remain unclear. We already reported that the intestinal calcium absorption is increased in MyD patients due to the elevation of plasma 1, 25 (OH) 2 D level. We also reported that serum immunoreactive parathyroid hormone (iPTH) levels and Nephrogenous cyclic AMP (NcAMP) levels are increased in MyD patients. This study was designed to elucidate the mechanism of hyperparathyroid state in MyD patients.
    Intravenous calcium tolerance test was performed in 7 patients with MyD and 7 control subjects, 3 patients with other neuromuscular disorder and 4 healthy subjects. Calcium was stepwisely infused at the concentration of 0,104.7,194.9 and 235.5mg every hour.
    The basal plasma calcium levels were significantly higher in MyD (9.79 ± 0.27mg/dl, Mean ± SD) as compared with control subjects (9.50±0.19; p<0.05). Basal serum iPTH levels were also significantly higher in MyD (514.0±188.9pg/ml) than those in control subjects (333.7±113.5; p<0.05).
    After calcium infusion, serum calcium levels were increased in both groups, but the levels of serum calcium remained significantly higher in MyD than those in control subjects. On the other hand, urinary calcium excretion levels were not different between the two groups. At the same time, %TRP and calcium clearance were significantly lower in MyD than control subjects.
    In spite of larger increments of serum calcium level after 235.5mg/h of calcium infusion in MyD (MyD 2.32±0.63mg/dl, control 1.84±0.59), the levels of serum iPTH in MyD remained significantly higher than control subjects (MyD 367.14±134.10pg/ml, control 175.43±67.57; p<0.01). Suppressibility of serum iPTH and NcAMP were decreased in MyD (27.1±13.9% and 58.8± 25.2, respectively) as compared with control subjects (41.1 ±7.1% and 69.6 ± 24.2, respectively).
    Therefore, the regulation of iPTH level by serum calcium seems to be less sensitive in MyD. This might be the reason why urinary calcium excretion levels were not different between the two groups while serum calcium levels were higher in MyD.
    It may be concluded that MyD patients are in a state of hyperparathyroidism, and this might be due to the insensitivity of the control mechanism of parathyroid hormone secretion by serum calcium level.
  • 視床下部性肥満マウスを用いての検討
    西岡 均, 吉田 俊秀, 吉岡 敬治, 近藤 元治
    1988 年 64 巻 7 号 p. 554-563
    発行日: 1988/07/20
    公開日: 2012/09/24
    ジャーナル フリー
    This study was designed to clarify the role of the ventromedial hypothalamus (VMH) in the regulation mechanism of sympathetic nervous system (SNS) activity. In obese mice with chemically destroyed VMH, norepinephrine (NE) turnover, which is a reliable indicator of SNS activity, was measured in the interscapular brown adipose tissue (IBAT) and heart using inhibition of NE biosynthesis with α-methyl-p-tyrosine; the core temperature was also measured. Two types of hypothalamic obese mice (monosodium glutamate (MSG) -treated mice and gold thioglucose (GTG) -treated mice) were used under two diverse conditions : overfeeding and acute cold exposure. The former was performed via sucrose addition, and the latter was carried out at 6°C in two groups of obese mice and their controls.
    A comparison between the overfed mice and those fasted for 48 hours revealed that the fasted normal controls showed significantly lower core temperatures and significantly decreased NE turnover in the IBAT and heart as compared with the overfed normal controls, while no significant differences were observed between overfed and fasting obese mice in core temperature or NE turnover. Another comparison disclosed that the core temperatures were significantly lowered and NE turnover in both organs increased significantly after cold exposure in two obese groups and their normal controls, though there were no noticeable differences between the MSG- or GTG-treated mice and their controls. These results indicate that the VMH is a center of SNS for response to feeding but not for response to cold.
  • 浜崎 信一郎, 梅田 照久, 岩岡 大輔, 直海 晶二郎, 大野 美保, 三浦 史博
    1988 年 64 巻 7 号 p. 564-572
    発行日: 1988/07/20
    公開日: 2012/09/24
    ジャーナル フリー
    The pathophysiological role of the central dopaminergic mechanism in human essential hypertension (EH) is still unknown. We studied on the relationship between the dopaminergic activity and the salt-sensitivity. Twenty three hospitalized patients with EH were divided into the salt-sensitive group (SS, n=12) or non salt-sensitive group (NSS, n=11) by their responses whether they caused more than 8% increase in mean blood pressure (MBP) when the dietary salt was increased from 2g/day to 20g/day for 7 days of each. The change of central dopaminergic activity by the salt load was evaluated by the decrement of plasma prolactin (PRL) response to small dosage (25μg) of thyrotropin releasing hormone. The mean percent change of PRL response by the salt load in the SS group was -6.5±8.3% (mean-±SEM), which was significantly lower than 26.8±5.5% in the NSS group (p<0.01). There was a significant negative correlation between the percent changes of PRL response and the percent changes of MBP by the salt load (r=-0.448, p<0.05). These results suggested that the rise in blood pressure by salt load in SS patients with EH might be due to a reduced activity of the central dopaminergic mechanism.
  • 山谷 金光, 二川原 和男, 鈴木 唯司, 舟生 富寿, 五十嵐 隆子, 寺山 百合子
    1988 年 64 巻 7 号 p. 573-581
    発行日: 1988/07/20
    公開日: 2012/09/24
    ジャーナル フリー
    To study the relation of normetanephrine (NM) and metanephrine (M) to norepi-nephrine (NE) and epinephrine (E), plasma free NM (f-NM), free M (f-M), total NM (t-NM) and total M (t-M) were measured in normal subjects and patients with pheochromocytoma (PHEO), neuroblastoma, Cushing's syndrome, primary aldosteronism and chronic renal failure (CRF) by radioimmunoassay. Plasma f-NE and E were measured by radioenzymatic assay.
    Both f- and t-NM were high in PHEO, neuroblastoma and CRF. f- and t-M were also high in some patients with PHEO and CRF. Positive correlation was observed not only in f-NE with f-NM and t-NM, but also in f-E with f-M and t-M except for CRF. Although up-right posture induced an elevation in f-NE and f-NM, t-NM was unchanged in normal subjects. In patients with PHEO, metochlopramide induced a prompt elevation in f-NE and E but no-change in t-NM and M levels. f-NE, f-E, f-NM, t-NM, f-M and t-M decreased rapidly after the resection of PHEO and reached the normal level on the third day after the surgery. In CRF patients, f-NM, t-NM, f-M and t-M decreased after hemodialysis despite an increase of f-NE.
    From these results, it was suggested that plasma NM and M levels reflected plasma NE and E to a certain extent in normal subjects and patients with normal renal function, and that the impaired renal function provoked an elevation of plasma NM and M due to the accumulation of them.
  • 今井 龍幸, 伊在井 みどり, 成宮 成利, 永木 正仁, 足立 定司, 大平 敏樹, 上久保 啓太, 塩岡 誠, 藤岡 均, 琴尾 泰典, ...
    1988 年 64 巻 7 号 p. 582-592
    発行日: 1988/07/20
    公開日: 2012/09/24
    ジャーナル フリー
    A case of pseudo-Bartter's syndrome associated with hypokalemic myopathy was presented.
    A 37-year-old housewife was admitted to our hospital because of muscle cramps with muscle weakness and tetany. There was a history of facial edema and constipation, which have been managed with “Kampomedicine (Chinese medicine)” and laxatives for several years. The patient was amenorrhea 3 months before entry. She began to experience muscle weakness and muscle cramps associated with gait disturbance 2 or 3 months before admission. On physical examination, she was thin with positive Trousseau's and Chvostek's signs. Laboratory studies revealed hypokalemia, low urinary excretion of potassium, hypo-calcemia, metabolic alkalosis, elevated creatine phosphokinase (CPK), increased levels of plasma renin activity and plasma aldosterone concentration, and decreased sensitivity to pressor effect of angiotensin II. Potassium supplementation resulted in restoration of her symptomes and normalization of low serum calcium and elevated CPK levels. She was diagnosed to be pseudo-Bartter's syndrome due to anorexia nervosa.
    The mechanism (s) of hypokalemia in our case was discussed.
  • 伊原 利和, 宮地 幸隆
    1988 年 64 巻 7 号 p. 593-605
    発行日: 1988/07/20
    公開日: 2012/09/24
    ジャーナル フリー
    Tissue distribution of epinermal growth-factor (EGF) in rat was investigated using a human EGF (hEGF) radioimmunossay system.
    Antisera generated against hEGF reacted with hEGF and [21 Leu] hEGF but not with mouse EGF, fibroblast growth factor (FGF), nerve growth factor (NGF), platelet derived growth factor (PDGF), and endothelial cell growth supplement (ECGS).
    Similar amounts of EGF immunoreactivity (EGF-IR) were found in the rat submandibular gland (32.8±4.59ng/g tissue, n= 5) and duodenum (39.9± 18.7ng/g tissue, n= 9), whereas little EGF was detected in other tissues. No sex difference was observed in submandibular and duodenal EGF-IR, being different from the case of mouse in which ten times higher concentration of EGF-IR was found in male submandibular gland. Sephadex G-50 gel chromatography of submandibular and duodenal extracts revealed that each consisted of at least three different immunoreactive forms. The predominant EGF-IR was coeluted with 125 I-EGF, significant amounts of EGF-IR was observed in the void volume fractions, and only small peaks of EGF-IR were present near Vt.
    These data clarified the presence of EGF-IR in rat submandibular and duodenal tissues and the molecular heterogeneity of EGF-IR and suggest some important role of EGF in the gastrointestinal function.
  • 小崎 俊男, Carol Yarborough, 大沢 由男
    1988 年 64 巻 7 号 p. 606-622
    発行日: 1988/07/20
    公開日: 2012/09/24
    ジャーナル フリー
    We reported on the unusually high isotope effect of non-aromatizing androgen 19- hydroxylase in sheep and dog adrenals and the validity of the [3H] water method using [19-3H3] androgen. We have extended the study to examine whether this 19-hydroxylation is catalyzed by a cytochrome P-450 dependent enzyme. Sheep adrenal homogenate (1.65mg prot.) was incubated in the presence of NADPH (5.6mM) with [19-3 H3, 4-14 C] -andro-stenedione (A) (3.2μM, 8.24 × 104 dpm 3H/μg, 3 H/14 C = 17.2) in a total of 1.2ml PO4 buffer under air at pH 7.4 for 2, 5 and 10 min. [19-3 H2, 4-14C] -19-hydroxy-A (19-OHA) with added carrier was purified through extraction, TLC, acetylation to form 19-AcOA, and further TLC to give 19-hydroxylase activity as assessed by the product isolation method. Simultaneously, the [3 H] water was measured by distillation, and with correction by the apparent kinetic isotope effect (KH/KT=11.8), used for assessment of 19-hydroxylase activity. The effects on the hydroxylation by cofactor (NADPH, NADH), incubation atmosphere (N2, CO/O2), cytochrome P-450 inhibitors (metyrapone, clotrimazole) and heating were measured by both methods. Compared to the complete system (89.6pmol/min/mg as 100%), carbon monoxide suppressed 15.8, 59.3 and 86.4% of the 19-hydroxylation when a CO/O2 ratio of 0.1, 1 and 9 was used, respectively. Replacement to nitrogen atmosphere decreased the activity by 93.8%. Replacement of NADPH with NADH (7.5mM) caused more than a 92.1% decrease in activity. Metyrapone at 50 and 200μM and clotrimazole at 2.5 and 10μM suppressed the activity by 82.8, 90.4, 85.4 and 94.9%, respectively. A larger scale sheep adrenal incubation of A (250μM) under 18 O2 atmosphere and isolation of 19-AcOA were carried out in a similar manner. The gas chromatography-mass spectrometry analysis of the purified product showed 48.5% of the product to be 18 O-labeled as [M+ + 2], m/e 346. Thus, the non-aromatizing androgen 19-hydroxylase requires NADPH and molecular oxygen. It is strongly inhibited by carbon monoxide and cytochrome P-450 inhibitors. These results indicate that the enzyme system responsible for non-aromatizing androgen 19-hydroxylase in adrenal is a cytochrome P-450 dependent monooxygenase. This research was supported in part by USPHS NIH RESEARCH GRANT HD 18792.
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