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57 巻, 9 号
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鳥居 隆三, 宇津 佐知子, 谷岡 功邦1981 年 57 巻 9 号 p. 1177-1185
発行日: 1981/09/20
公開日: 2012/09/24
ジャーナル フリーIt was reported previously that marmoset monkeys have extremely high plasma levels of unconjugated cortisol in resting as well as ACTH-stimulated conditions. These findings led us to investigate whether or not marmoset monkeys show the symptoms of Cushing's syndrome. Twenty-three adult marmoset monkeys (cotton topped tamarins) were used with 49 adult rhesus monkeys as controls. Serum total corticoids were measured by a competitive protein binding assay, serum aldosterone by a radioimmunoassay, and glucocorticoid receptor in the liver was determined by a radioreceptor assay.
The standard dexamethasone suppression test (0.04 mg/kg/day × 2, 0.16 mg/kg/day × 2) revealed proper suppression in the rhesus monkeys but no suppression in the marmosets. The latter finding is similar to the situation observed in Cushing's syndrome in man and suggests poor suppression of pituitary ACTH by the excessive glucocorticoids. The adrenocortical histology showed hyperplasia of fasciculata and reticularis cells. The hemogram and blood chemistry in the marmoset monkeys were similar to those in the rhesus monkeys, except for hyperglycemia. The mean resting serum aldosterone level was higher than that in both man and in the rhesus monkey. No hypokalemia was found. It has been reported that marmoset monkeys show extremely high plasma levels of estrogen and progesterone without any clinical symptoms due to the excess of these hormones.
Thus, in the present experiment it was found that the pituitary-adrenocortical relationship in the marmoset monkeys seemed to be compatible with that in Cushing's syndrome in man but was not accompanied by any clinical symptoms due to excessive cortisol.
This may suggest that this unresponsiveness to cortisol in marmoset monkeys is derived from the small amount of glucocorticoid receptor and presumably from the lower function of the post receptor system.抄録全体を表示PDF形式でダウンロード (963K) -
徳弘 悦郎, 諏訪 城三1981 年 57 巻 9 号 p. 1186-1198
発行日: 1981/09/20
公開日: 2012/09/24
ジャーナル フリーAdrenal androgen is thought to take part in the expression of secondary sexual characteristics and growth spurt with the onset of puberty. Its secretion is known to rise prior to the increase of gonadotropin and gestagen secretion in the pubertal period. But there are many unsolved problems concerning its physiological activity and the regulation of its secretion. To investigate these problems, we measured serum dehydroepiandrosterone sulfate (DHEA-S) in normal children and 41 patients with pituitary dwarfism and analyzed the relation of serum DHEA-S levels to puberty, growth and pituitary function.
Serum DHEA-S was measured by RIA modified by Buster's method. Serum DHEA-S levels of normal children started to rise after 6 years of age, and rapidly increased over 9 years. Serum DHEA-S levels were well correlated with urinary 17-KS excretion (r=0.85) and increased by ACTH stimulation (basal 54.4 ± 36.8 μg/dl, 4 hrs after ACTH-Z i.m. 86.2 ± 59.4 μg/dl in children over 9 years).
Serum DHEA-S levels in 18 out of 26 cases of pituitary dwarfism over 9 years were definitely below normal. 5 cases who had normal ACTH, prolactin and gonadotropin secretion showed pubertal change and a rapid increase in serum DHEA-S levels during two and a half years of hGH treatment. 2 cases who had normal ACTH and prolactin secretion but were gonadotropin deficient showed a remarkable increase in serum DHEA-S levels without pubertal change. 13 cases with ACTH deficiency showed low levels of serum DHEA-S and no pubertal change with the exception of 1 case. 6 cases with prolactin deficiency and normal ACTH secretion also showed low serum DHEA-S levels. DHEA-S secretion seems to be related to GH, ACTH and prolactin.
During hGH-only treatment and treatment with hGH plus low doses of anabolic steroid (Stanozolol), changes in growth rate were compared among 3 cases with normal serum DHEA-S levels and 10 cases with low serum DHEA-S levels over 9 years. The growth rate of the low DHEA-S group exhibited a waning effect during hGH-only therapy and returned to the optimal growth rate with hGH plus a low dose Stanozolol. The normal DHEA-S group showed a good response to the hGH-only therapy and no remarkable change during the two types of treatment.
These observations suggest that adrenal androgen deficiency exists in many cases of pituitary dwarfism and that supplemental therapy may be needed for hGH to exert its full effect. Serum DHEA-S can be an index of adrenal androgen secretion.抄録全体を表示PDF形式でダウンロード (933K) -
河村 寛, 田中 孝, 三好 秋馬, 加藤 浩二, 宮地 幸隆1981 年 57 巻 9 号 p. 1199-1208
発行日: 1981/09/20
公開日: 2012/09/24
ジャーナル フリーOccupancy of luteinizing hormone (LH) /human chorionic gonadotropin (hCG) receptors in testes by LH or hCG is followed by stimulation of 3' : 5'-cyclic AMP (cAMP) production and testosterone synthesis. However, recently a sustained loss of testicular LH/hCG receptors after systemic administration of LH or hCG has been observed. Therefore we studied the functional relations between negative regulation of LH/hCG receptors and desensitization of cAMP and steroidogenic responses in the testes of rats treated with exogenous gonadotropin.
Adult male rats (200-250gr) were orchiectomized everyday for a week after an intraperitoneal injection of 20 or 200IU of hCG. The LH/hCG receptors in the testes were determined by incubating 50mg testis slice with 125I-hCG in the absence or presence of hCG. The effects of hCG pretreatment on cAMP and testosterone responses to the in vitro addition of hCG were also investigated.
The specific binding of 125I-hCG to LH/hCG receptors dropped rapidly to undetectable level at 24hr after 2001U hCG, remained undetectable for 3 days and began to recover at 4 days. After 20IU hCG, the specific binding of 125I-hCG did not decline up to 24hr, then fell to 44-68% at 2 days, and began to recover at 3 or 4 days. Scatchard analysis showed that the reduced binding of 125 125I-hCG was due to a reduction in the number of receptor sites without any change in affinity. These findings demonstrate that the hCG-induced change in testicular LH/hCG receptor is characterized by a progressive and dose-related loss of the receptors.
Pretreatment with both 20 and 2001U of hCG caused a marked increase in basal testosterone production in vitro at 24hr, but the testosterone responses to the addition of hCG in vitro were minimal at 24hr and recovered at 2 and 3 days after 20 and 200IU of hCG, respectively. Thereafter the testosterone responses increased 3 to 6 folds above those of intact rat testis. hCG-induced cAMP production in vitro was inhibited markedly at 24hr after 20 and 200IU hCG injection. Then the cAMP responses to hCG recovered gradually and were the same as those of the control after 4 days when testosterone responses were still high. This marked disparity between the recoveries of cAMP and testosterone responses after hCG treatment suggests that the testosterone synthetic enzymes located beyond cAMP formation are activated as a result of direct and delayed hCG action.
Another interesting point is that both testosterone and cAMP responses to hCG at 24hr after 20IU hCG were reduced to 11-31% of the control without a reduction in LH/ hCG receptors. This finding indicates that the initial block in steroidogenic responses to a small amount of hCG is not an immediate consequence of receptor loss, but must be located in the steps between LH/hCG receptor and cAMP formation.
These studies have shown that the responses of target cells after hCG injection undergo a series of changes; the desensitization and recovery of testis function. The earliest change seems to be rapid loss of cAMP response to hCG and then the dose-related loss of the free hCG receptors occurs. The elevated testosterone response to hCG is the late effect of hCG.抄録全体を表示PDF形式でダウンロード (805K) -
第一編 Competitive Protein Binding Assayによる血中25-OH-D測定の検討土光 茂治, 森田 陸司, 福永 仁夫, 山本 逸雄, 滋野 長平, 山本 厚江, 鳥塚 莞爾1981 年 57 巻 9 号 p. 1209-1222
発行日: 1981/09/20
公開日: 2012/09/24
ジャーナル フリーA simple and precise method has been developed for the determination of 25-hydroxyvitamin D in 1 ml of human plasma. The method consists of methanol/choloroform extraction, purification by high pressure liquid chromatography and a competitive protein binding assay using vitamin D deficient rat serum. The ethanol extract from vitamin D deficient chick serum was added to the sample before CPBA to eliminate the non-specific interference in the CPBA system as a vitamin D free serum extract. The assay was sensitive to 0.72 ng/ml of plasma. Satisfactory results were obtained in the dilution and recovery tests. The coefficients of variation were 5.8-9.1% for the within-assay, and 7.4-10.3% for the between-assay. Plasma concentrations of 25-hydroxyvitamin D in 46 samples of normal human plasma were 21±10.5 ng/ml (mean±SD), and the seasonal variation was demonstrated. Plasma levels for 25-hydroxyvitamin D were high in patients receiving vitamin D2 and low in patients suffering from liver cirrhosis.抄録全体を表示PDF形式でダウンロード (1078K) -
第二編 諸種vitamin D誘導体の同一試料からの同時測定に関する基礎的研究土光 茂治, 森田 陸司, 福永 仁夫, 山本 逸雄, 山本 厚江, 滋野 長平, 山田 和代, 鳥塚 莞爾1981 年 57 巻 9 号 p. 1223-1238
発行日: 1981/09/20
公開日: 2012/09/24
ジャーナル フリーWe described a specific and reliable method for the simultaneous measurement of four groups of vitamin D derivatives in 5ml of plasma using a high-pressure liquid chromatography (HPLC) and a competitive protein binding assay (CPBA). The fraction of vitamin D (v.D), 25-hydroxy vitamin D (25-OH-D), 24, 25-dihydroxy vitamin D3 [24, 25- (OH) 2D3] and 1, 25-dihydroxy vitamin D3 [1, 25- (OH) 2D3] were separated from a methanol extract of a 5 ml plasma sample by HPLC using a silicic acid column (Zorbax SIL : 0.64 × 25 cm) and repurified by a reverse phase of HPLC on Zorbax ODS. Then the v.D2, v.D3, 24-OH-D2, 25-0H-D2, 25-OH-D3 and 24, 25- (OH) 2O3 were quantified by its absorbtion at 254 nm (HPLC assay). After the HPLC procedure, the 25-OH-D3, 24, 25- (OH) 2 D3 and 1, 25- (OH) 2D3 fractions were applied to CPBA. There was a good agreement between the values measured by the HPLC assay and by CPBA for plasma 25-OH-D3 (r=0.97) and in plasma 24, 25- (OH) 2D3 (r=0.98). More than 79% of the labeled vitamin D metabolites initially added to test plasma were recovered through the entire procedure. In the present assay, the detection limits of v.D3, 25-OH-D3, 24, 25- (OH) 2 D3 and 1, 25- (OH) 2 D3 were 1.21, 0.72, 0.12 and 0.0006 ng/ml (plasma) respectively. The variation of coefficients (CV) in the HPLC assays of v.D3, 25-OH-D3 and 24, 25- (OH) 2D3 were 4.9, 5.0 and 26.1% for the within-assay and 9.4, 5.5 and 30.0% for the between-assay. CV in CPBA of 25-0H-D3, 24, 25- (OH) 2 D3 and 1, 25- (OH) 2 D3 were 6.5, 8.2 and 8.3% for the within-assay and 10.2, 9.8 and 10.5% for the between-assay. The results of the dilution and recovery experiments were satisfactory, indicating that the present technique measures endogenous v.D3 derivatives correctly and accurately.
In 51 normal Japanes (aged 3 to 42), the plasma concentration of v.D2 was less than 10 ng/ml, v.D3 was less than 31 ng/ml, 25-OH-D2 was less than 20 ng/ml, 25-OH-D3 was 5-61 ng/ml, 24, 25- (OH) 2 D3 was 0.5-2.5 ng/ml and 1, 25- (OH) 2 D3 was 6-52 pg/ml.抄録全体を表示PDF形式でダウンロード (1200K) -
弓田 滋, 海上 寛, 孫 孝義, 古川 洋太郎1981 年 57 巻 9 号 p. 1239-1246
発行日: 1981/09/20
公開日: 2012/09/24
ジャーナル フリーA 38-year-old woman was diagnosed as having pseudohypoparathyroidism on the basis of hypocalcemia (7.1 mg/dl), hyperphosphatemia (4.9 mg/dl) and elevated circulating immunoreactive parathyroid hormone (0.44 ng/ml, carboxy-terminal assay). After her admission, her serum calcium level unexpectedly returned to the normal value (8.8 mg/dl), where-as the serum phosphate level was still elevated (5.3 mg/di). Although the circulating immunoreactive parathyroid hormone was elevated (0.46 ng/ml), nephrogenous cyclic AMP was rather reduced (1.02 nmol/100 mlGF), which suggested renal resistance to the endogenous parathyroid hormone. All of the vitamin D metabolites levels such as 25-hydroxyvitamin D, 24, 25-dihydroxyvitamin D and 1, 25-dihydroxyvitamin D were within the normal range.
The oral administration of phosphate (3.0 g/day) easily produced a decrease in serum calcium level and tetany. Urinary phosphate and cyclic AMP excretions in response to the exogenous parathyroid hormone (Parathormone, Lilly) were higher than those in pseudohypoparathyroidism and lower than those in idiopathic hypoparathyroidism. The response of plasma cyclic AMP to Parathormone was higher than the response range of pseudohypoparathyroidisms and lower than that of idiopathic hypoparathyroidisms.
Since the patient manifested hypocalcemic tetany in the outpatient clinic, oral administration of 1, 25-dihydroxyvitamin D3 (1.5 μg/day) was tried, and it resulted in the normalization of serum calcium, serum phosphate and circulating immunoreactive parathyroid hormone with no tetany.
It is clear from these results that the present case had an endorgan resistance to the parathyroid hormone. However, her serum calcium level was within the normal range with the normal level of circulating 1, 25-dihydroxyvitamin D. This may be explained by the maximal stimulation of 25-hydroxyvitamin D-la-hydroxylation system with elevated endogenous parathyroid hormone. The present case may belong to the category of normocalcemic pseudohypoparathyroidism.抄録全体を表示PDF形式でダウンロード (686K)
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