日本内分泌学会雑誌
Online ISSN : 2186-506X
Print ISSN : 0029-0661
ISSN-L : 0029-0661
68 巻, 6 号
選択された号の論文の6件中1~6を表示しています
  • 松本 圭史
    1992 年 68 巻 6 号 p. 577-583
    発行日: 1992/06/20
    公開日: 2012/09/24
    ジャーナル フリー
    Estrogen and androgen play essential roles in the development of breast cancer and prostate cancer, respectively. However, only 30% of breast cancer mass and 70% of prostate cancer mass are found to be hormone-dependent when they have been treated clinically. These findings show that hormone dependency of cancer disappears rather easily.
    Recently, it has been found that the growth of hormone-dependent cancer is mediated through sex steroid-induced growth factors in an autocrine manner.
    Future studies on sex steroid-induced growth factor(s) will play important roles in order to understand the molecular mechanisms of the development and growth of breast cancer and prostate cancer.
  • 永山 雄二, 長瀧 重信
    1992 年 68 巻 6 号 p. 584-591
    発行日: 1992/06/20
    公開日: 2012/09/24
    ジャーナル フリー
    The molecular cloning of the thyrotropin (TSH) receptor cDNA has led to advances in understanding the structure and function of the molecule and the pathogenesis of autoimmune thyroid disease. The recombinant TSH receptors expressed on mammalian cells are now available for TSAb and TBIAb assays. TBI assay in this system is much more sensitive than the conventional method. The binding sites for TSH and TSAb/TBIAb have been studied with epitope library, synthetic peptides, anti-peptide sera and mutagenesis. Some of these data, however, are confusing and undefined. The binding sites for TSH and TSAb/TBIAb are very likely to span the entire region of the extracellular domain of the TSH receptor with discontinuous contact points, and seem to be different from each other on N-terminal half, but similar on C-terminal half, of the extracellular domain of the receptor. However, the determination of the precise amino acids involved may be very difficult without monoclonal anti-TSH receptor antibodies.
  • -腎症の発症・増悪因子について-
    五味 由加利, 鈴木 晟時, 牧野 文則, 詫摩 哲郎, 細井 俊子, 近藤 弓子, 三倉 亮平, 飯野 史郎
    1992 年 68 巻 6 号 p. 592-599
    発行日: 1992/06/20
    公開日: 2012/09/24
    ジャーナル フリー
    Diabetic nephropathy is the most important complication of diabetes, because it is a major cause of morbidity and mortality for diabetic subjects. Since not all subjects with diabetes are at risk of developing this complication, we conducted a study to determine if heredity might be a possible risk factor for diabetic nephropathy in non-insulin dependent diabetes.
    Twenty-one factors including inheritance of nephropathy and hypertension were investigated in 109 individuals with NIDDM: 50 patients without proteinuria (Group I), 20 patients with intermittent proteinuria (Group II), and 39 patients with continuous proteinuria (Group III) matched for age and duration of diabetes. Of those patients, 55 patients with inheritance of diabetes were also divided into three groups: 29 patients without proteinuria (Group I), 9 patients with intermittent proteinuria (Group II), and 17 patients with continuous proteinuria (Group III).
    Individuals in Groups II and III has significantly higher frequency of inheritance of diabetic nephropathy than those in Group I, and also individuals with inheritance of diabetic nephropathy had significantly higher frequency of diabetic nephropathy than those without it. Frequency of hypertension, retinopathy and body mass index in the past were significantly higher in subjects in Groups II or Group III than in those in Group I. There were no significant differences between subjects in Groups II and III.
    These findings suggest that susceptibility to diabetic nephropathy in NIDDM may be hereditary, although hypertension and obesity may also be important risk factors for diabetic nephropathy.
  • 三村 明, 景山 茂, 伊藤 景樹, 三浦 順子, 蔵田 英明, 横山 淳一, 池田 義雄
    1992 年 68 巻 6 号 p. 600-606
    発行日: 1992/06/20
    公開日: 2012/09/24
    ジャーナル フリー
    The early morning hyperglycemia of diabetic patients has been commonly referred to as the“dawn phenomenon”. Recently the nocturnal surges of growth hormone (GH) have been suggested as an important factor in the pathogenesis of the dawn phenomenon. In order to reassess the role of the nocturnal GH secretion in the dawn phenomenon, seven C-peptide negative diabetic patients were studied during 48hr-feedback control using a closed-loop insulin infusion device (Biostator®). They received oral sleeping medication only on the first night (control) and sleeping medication with anticholinergic agent (pirenzepine 75mg) on the second night, and blood glucose, insulin requirements, GH and cortisol concentrations during 0000hr and 0700hr were measured. The peak of sleep-induced GH secretions was markedly suppressed by pirenzepine in comparison with the control night (19.8±3.7 vs. 3.0±1.2ng/ml; p<0.05). Insulin requirements during 0500hr and 0700hr were suppressed significantly by pirenzepine (3.0±0.2 vs. 2.0±0.2U/2hr; p<0.05). Insulin infusion ratio, i. e. insulin requirements during 0500hr and 0700hr divided by those during 0000hr and 0200hr, was decreased by pirenzepine (2.2±0.3 vs. 1.5±0.2; p<0.05). There were no significant differences in blood glucose and cortisol concentrations whether or not the anticholinergic agent was given. In conclusion, these results have shown that an anticholinergic agent may be useful in the management of insulin-treated patients with marked dawn phenomenon.
  • -クッシング病とクッシング症候群との対比を中心として-
    小宮 一郎, 高須 信行, 小原 範子, 長澤 慶尚, 大塚 弘巳, 浅輪 孝幸, 山田 隆司
    1992 年 68 巻 6 号 p. 607-622
    発行日: 1992/06/20
    公開日: 2012/09/24
    ジャーナル フリー
    We experienced 41 cases of Cushing's syndrome (12 males and 29 females, 15 years old-65 years old) during the last 20 years. These included 20 patients with unilateral adrenal adenoma (Cushing's syndrome), 19 patients with bilateral adrenal hyperplasia (Cushing's disease), one patient with adrenal carcinoma and one patient with primary adrenocortical nodular dysplasia (PAND). Moreover, these cases included some special ones, i. e. 5 cases with destructive thyroiditis after treatment, 2 cases with aggravation of arthritis after treatment, a case of Carney's complex with PAND, one case with paradoxical response to dexamethasone, and one case combined with empty sella syndrome.
    The most specific clinical signs were moon face (95% occurrence), hypertension (95%) and subcutaneous bruising (80%). Other significant signs were eye edema (66%), buffalo hump (68%), subcutaneous purpura (63%) and osteoporosis (49%). Skin striae was not a common sign in our cases (41%). Renal stone was observed in only 20% of our patients but was a significant sign in this syndrome. There was no difference in the occurrence of each clinical sign between Cushing's syndrome and Cushing's disease. The elevation of white blood cell count (WBC) and serum sodium, a decrease of serum potassium, and a decrease of reabsorption of phosphate (%TRP) were observed.
    Thyroid-stimulating hormone (TSH) and human growth hormone (HGH) were suppressed in patients with Cushing's syndrome and patients with Cushing's disease. These results were consistent with those of previous reports. However, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) were high in those patients with Cushing' s syndrome and those with Cushing's disease.
    Oral glucose tolerance test was carried out in 34 patients before and after treatment. Thirty-one percent of those had diabetes mellitus and 26% had impaired glucose tolerance (IGT). The response of IRI in this test was high in patients with Cushing's syndrome and patients with Cushing's disease, and decreased 4 weeks after treatment in those with Cushing's syndrome but remained high in those with Cushing's disease.
    Plasma ACTH level and urinary 17-OHCS excretion were significantly higher in Cushing's disease than in Cushing's syndrome. During an 8mg-high-dose dexamethasone suppression test, urinary 17-OHCS excretion in 13 of 14 patients with Cushing's disease (93%) was suppressed by more than 50% of baseline on the second day of testing. However, all of 18 patients with Cushing's syndrome, who had an 8mg-dexamethasone suppression test, failed to suppress urinary 17-OHCS by 50% of baseline.
    In other diagnostic procedures, abdominal CT-scan with quantitative analysis, and 131I-adosterol adrenal scintigraphy were very useful in establishing the definitive diagnosis of Cushing's syndrome and Cushing's disease. ACTH stimulation test, metyrapone test, and abdominal MRI (magnetic resonance imaging) were also useful but not necessary except in the diagnosis of difficult cases of Cushing's disease.
  • 第I報: 消化吸収試験および糖負荷試験による検討
    若林 茂
    1992 年 68 巻 6 号 p. 623-635
    発行日: 1992/06/20
    公開日: 2012/09/24
    ジャーナル フリー
    It is widely acknowledged that high viscosity water-soluble dietary fibers such as pectin and guar gum affect a lowering of blood glucose levels and a reducing of insulin secretion following a sugar load. However, as dietary fibers vary in origin and in chemical properties, their physiological functions differ as well. In this study the effects of Indigestible Dextrin (PF-C), a low viscosity, water-soluble dietary fiber obtained through acid and heat-treatment of potato starch, on various aspects of sugar tolerance were examined.
    First, the influence of PF-C on sucrose hydrolysis was examined in rat intestinal mucosa cell homogenate confirming that PF-C did not inhibit sucrase activity. Then, in order to investigate the influence of PF-C on sugar digestion-absorption, an experiment was performed by using the everted intestinal sac of the rat in vitro. PF-C did not have an effect on glucose-transport into the serosal medium, whereas PF-C did inhibit the transport of hydrolyzed-glucose from sucrose, with no change in the hydrolysis of sucrose.Recently, Crane et al. reported that there is a specific route for hydrolyzed glucose from sucrose in glucose-absorption on the enteric surface (disaccharidase related transport system). The possibility exists that PF-C specifically affects this pathway. Further, total glucagon released into the serosal medium stimulated by both glucose and sucrose were reduced by PF-C.
    On the basis of these results, an oral sugar tolerance test was conducted in both rats and healthy human subjects. In male Sprague-Dawley rats (8 weeks old, 250-280g) concurrent administration of PF-C (0.6g/kg body weight) reduced an increase in plasma insulin levels with no change in glucose levels following a glucose (1.5g/kg body weight) load. Further noted were reductions in increases in both plasma glucose and insulin levels following a sucrose (1.5g/kg body weight) plus PF-C (0.6g/kg body weight) load to that of the sucrose (1.5g/kg body weight) single load. These findings reflect the above mentioned in vitro results. Moreover, in healthy male subjects the increase in both plasma insulin and glucagon-like immunoreactivity (Gut GLI) levels following a Trelan-G75 load were significantly reduced by concurrent administration of PF-C.
    From these observations it would appear that the effectiveness of reducing insulin secretion by PF-C results due to the decrease in sugar absorption by inhibiting the disaccharidase-related transport system. As glucagon-like peptide 1 (GLP-1), [an incretin in the enteroinsular axis] secreted with Gut GLI from intestinal L cells, is known to enhance insulin secretion following a sugar load, the resulting effectiveness by PF-C to reduce insulin secretion is thought to be attributed to the action on this enteroinsular axis mechanism.
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