Experimental and clinical endocrinology最新文献

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Plasma aldosterone response to metoclopramide in patients with Cushing's disease. 库欣病患者血浆醛固酮对甲氧氯普胺的反应
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211220
S Zacharieva, I Stoeva, P Matrozov, K Andonova
{"title":"Plasma aldosterone response to metoclopramide in patients with Cushing's disease.","authors":"S Zacharieva, I Stoeva, P Matrozov, K Andonova","doi":"10.1055/s-0029-1211220","DOIUrl":"https://doi.org/10.1055/s-0029-1211220","url":null,"abstract":"The acute effect of metoclopramide on aldosterone and prolactin levels were studied in 8 control subjects and 11 patients with Cushing's disease. Metoclopramide (10 mg i.v.) induced a similar plasma prolactin response in control subjects and patients. No difference was found in basal aldosterone levels between the two groups. Apart from a more delayed aldosterone response to metoclopramide in the Cushing's disease group, no significant difference in the peak aldosterone values was found between the patients and controls. The short-term treatment with DA2-receptor agonist bromocriptine was without effect on aldosterone response to metoclopramide in the Cushing's disease group. These results argue against an altered dopaminergic control of aldosterone secretion in patients with Cushing's disease. The lack of a bromocriptine effect on aldosterone response to metoclopramide is in accordance with the concept that the dopamine receptors involved in aldosterone regulation differ from classical DA2 receptors.","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 3","pages":"138-43"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211220","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19213034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
BGP serum levels in patients with thyroid carcinoma before and 4-14 weeks after radioiodine therapy. 放射性碘治疗前后4-14周甲状腺癌患者血清BGP水平的变化。
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211229
H Stracke, K Federlin
{"title":"BGP serum levels in patients with thyroid carcinoma before and 4-14 weeks after radioiodine therapy.","authors":"H Stracke,&nbsp;K Federlin","doi":"10.1055/s-0029-1211229","DOIUrl":"https://doi.org/10.1055/s-0029-1211229","url":null,"abstract":"<p><p>In the present short paper we compared the BGP and AP levels of 26 patients with thyroid carcinoma during radio-iodine therapy. BGP values reflect the bone turnover before and after radio-iodine therapy. There were no significant AP changes during this period. These results suggest that thyroid hormone has a direct effect on osteoblast function and that this effect can be best monitored by determination of BGP levels.</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 3","pages":"186-8"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211229","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19213532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of angiotensin II and atrial natriuretic peptide on LH release are exerted in the preoptic area: possible involvement of gamma-aminobutyric acid (GABA). 血管紧张素II和房利钠肽对视前区LH释放的影响:可能与γ -氨基丁酸(GABA)有关。
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211256
P Rodriguez Lopez, A Ehlerding, S Leonhardt, H Jarry, W Wuttke
{"title":"Effects of angiotensin II and atrial natriuretic peptide on LH release are exerted in the preoptic area: possible involvement of gamma-aminobutyric acid (GABA).","authors":"P Rodriguez Lopez,&nbsp;A Ehlerding,&nbsp;S Leonhardt,&nbsp;H Jarry,&nbsp;W Wuttke","doi":"10.1055/s-0029-1211256","DOIUrl":"https://doi.org/10.1055/s-0029-1211256","url":null,"abstract":"<p><p>The preoptic/anterior hypothalamic area (PO/AH) contains the majority of LHRH neurons of which the function is regulated by a variety of neurotransmitters and peptides. In this area, numerous estrogen-receptive neurons utilize gammaaminobutyric acid (GABA) as neurotransmitter and these neurons communicate directly with LHRH neurons. Angiotensin II (AII) and atrial natriuretic peptide (ANP) are known to be involved in the regulation of LH secretion. The site of action of these peptides and the mechanisms by which they influence LHRH neurons, are largely unknown. Therefore the effects of intrapreoptic application of AII and ANP on serum LH levels of ovariectomized (ovx) and of ovx estrogen-primed rats were investigated. The peptides were applied into the PO/AH by means of push-pull cannula and in the effluent fractions GABA was measured. In the ovx estrogen-primed rat, prominent LH and prolactin surges were observed. At the time of increased LH levels preoptic GABA release was significantly reduced. At this time application of AII or ANP into the PO/AH was without effect on either LH or prolactin levels in the serum or on preoptic GABA release rates. In ovx, not steroid-primed rats intrapreoptic AII application suppressed serum LH levels significantly and this treatment had a slight stimulatory effect on preoptic GABA release rates. This effect of AII could be antagonized by prior preoptic treatment with saralasin, a specific AII receptor blocking peptide. Preoptic treatment with ANP resulted in a slight increase in serum LH levels which was accompanied by a slight, but significant reduction of preoptic GABA release rates.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 6","pages":"350-5"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211256","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19148390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Cyclic AMP formation in rat bone and kidney cells is stimulated equally by parathyroid hormone-related protein (PTHrP) 1-34 and PTH 1-34. 甲状旁腺激素相关蛋白(PTHrP) 1-34和PTH 1-34均可刺激大鼠骨和肾细胞中环状AMP的形成。
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211222
E Blind, F Raue, V Knappe, J Schroth, R Ziegler
{"title":"Cyclic AMP formation in rat bone and kidney cells is stimulated equally by parathyroid hormone-related protein (PTHrP) 1-34 and PTH 1-34.","authors":"E Blind,&nbsp;F Raue,&nbsp;V Knappe,&nbsp;J Schroth,&nbsp;R Ziegler","doi":"10.1055/s-0029-1211222","DOIUrl":"https://doi.org/10.1055/s-0029-1211222","url":null,"abstract":"<p><p>Parathyroid hormone-related protein (PTHrP) plays a major role in the pathogenesis of humoral hypercalcemia of malignancy. It interacts with the PTH receptor and has therefore a nearly identical effect on bone cells as PTH. However, PTHrP is thought to be less potent than PTH in stimulating adenylate cyclase in canine renal membranes, leading to the hypothesis of a differential efficiency in signal transduction by PTHrP with respect to bone vs kidney. In a homologous model with intact osteoblast-like cells (UMR 106) and primary kidney cells, both from the rat, we have tested N-terminal peptide fragments, based on the rat amino acid sequence 1-34, of PTH and PTHrP. Compared with PTHrP(1-34), rat PTH(1-34) had a similar relative potency in bone cells (85%) and in kidney cells (140%) in its ability to stimulate adenylate cyclase. Human PTH(1-34) was 5.6- to 6.5-fold less potent than rat PTH(1-34) in both cell types. In human osteoblast-like cells (SaOS-2), rat and human PTH were essentially equally potent compared to PTHrP(1-34) (identical sequence in rat and human) in stimulating cAMP accumulation. In conclusion, our study revealed the equipotency of rat PTH(1-34) and PTHrP(1-34) in stimulating intracellular cAMP formation in a homologous system of rat bone and kidney cells. There seemed to be no unique signal transduction mechanism of PTHrP to the adenylate cyclase in rat kidney cells compared with bone cells.</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 3","pages":"150-5"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211222","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19213036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 20
Relationship between the monoamine and gonadotropin content in follicular fluid of preovulatory graafian follicles after superovulation treatment. 超排卵治疗后卵泡液单胺与促性腺激素含量的关系
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211227
J Bódis, G Hartmann, A Török, Z Bognár, H R Tinneberg, P Cledon, V Hanf
{"title":"Relationship between the monoamine and gonadotropin content in follicular fluid of preovulatory graafian follicles after superovulation treatment.","authors":"J Bódis,&nbsp;G Hartmann,&nbsp;A Török,&nbsp;Z Bognár,&nbsp;H R Tinneberg,&nbsp;P Cledon,&nbsp;V Hanf","doi":"10.1055/s-0029-1211227","DOIUrl":"https://doi.org/10.1055/s-0029-1211227","url":null,"abstract":"<p><p>Noradrenaline (NA), serotonin (5HT), dopamine (DA), FSH, LH and prolactin (PRL) content was determined in 104 preovulatory follicular fluids obtained from 44 patients undergoing in vitro fertilization. The patients were given human menopausal gonadotropin (HMG) for ovarium stimulation, ovulation was induced with 10000 IU human chorionic gonadotropin (HCG) 34-36 hours prior to the follicular aspiration by vaginal ultrasound. Classification of the oocytes was performed by direct microscopic evaluation differentiating three groups of oocytes: Group I.: prophase I; Group II.: metaphase I; Group III.: metaphase II. There was no significant difference in monoamine and FSH content of follicular fluid at different stage of the oocyte maturation. LH and PRL significantly increased parallel with oocyte maturation (38.9; 48.8; 56.7 IU/l and 1324; 2382; 3134 IU/l). significant negative correlation was observed in Group I. between 5HT-LH (r = -0.64); in Group II. between NA-LH (r = -0.62) and NA-PRL (r = -0.51). Significant positive correlation were found in Group I. between FSH-LH (r = 0.63), in Group II. between LH-PRL (r = 0.56), in Group III. between NA-5HT (r = 0.66), NA-DA (r = 0.80) and 5HT-DA (r = 0.66). These observations suggest that action of LH and PRL may be negatively modulated by 5HT and NA in the final stage of oocyte maturation.</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 3","pages":"178-82"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211227","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19213530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 27
Familial glucocorticoid resistance: an overview. 家族性糖皮质激素抵抗:综述。
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211204
M Karl, G P Chrousos
{"title":"Familial glucocorticoid resistance: an overview.","authors":"M Karl,&nbsp;G P Chrousos","doi":"10.1055/s-0029-1211204","DOIUrl":"https://doi.org/10.1055/s-0029-1211204","url":null,"abstract":"Familial glucocorticoid resistance is an inherited form of generalized end-organ insensitivity to glucocorticoids, associated with qualitative and/or quantitative abnormalities of the glucocorticoid receptor. The glucocorticoid resistance syndrome is characterized by elevated plasma corticotropin (ACTH) and cortisol concentrations, set at higher levels but maintaining a circadian rhythm, and no clinical evidence of hypoor hypercortisolism. The clinical spectrum of this syndrome is broad, ranging from completely asymptomatic to mildly or severely symptomatic, characterized by manifestations of mineralocorticoid and/or androgen excess (Chrousos et al., 1982; Lamberts et al., 1986). The secretion of glucocorticoids is strictly regulated by an elaborate feedback system, the suprahypothalamic-hypothalamic-pituitary-adrenal-axis (SHPA) (Kellerwood and Dallman, 1984; Dallman et al., 1987; Jakobsen and Sapolsky, 1991): Corticotropin releasing hormone (CRH) and arginine vasopressin (AVP), secreted by the hypothalamus, stimulate the release of ACTH by the pituitary gland. ACTH then stimulates secretion of glucocorticoids by the adrenal cortex. Glucocorticoids exert negative feedback effects on the hippocampus, the hypothalamus and the pituitary, presumably via the classic (Type II) glucocorticoid receptor and/or the mineralocorticoid receptor (glucocorticoid receptor type I) (De Kloet, 1991). By Experimental and","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 1","pages":"30-5"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211204","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19461265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
The stimulatory effect of pituitary adenylate cyclase activating polypeptide (PACAP) on LH release from rat pituitary cells in vitro does not involve calcium mobilization. 垂体腺苷酸环化酶激活多肽(PACAP)对体外大鼠垂体细胞LH释放的刺激作用不涉及钙动员。
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211246
D Perrin, H D Söling, W Wuttke, H Jarry
{"title":"The stimulatory effect of pituitary adenylate cyclase activating polypeptide (PACAP) on LH release from rat pituitary cells in vitro does not involve calcium mobilization.","authors":"D Perrin,&nbsp;H D Söling,&nbsp;W Wuttke,&nbsp;H Jarry","doi":"10.1055/s-0029-1211246","DOIUrl":"https://doi.org/10.1055/s-0029-1211246","url":null,"abstract":"<p><p>The hypothalamic peptide \"pituitary adenylate cyclase activating polypeptide (PACAP)\" stimulates cAMP production in cultured rat pituitary cells and enhances LH release. It has been suggested that the stimulation of LH release by PACAP comprises two distinct mechanisms: a direct stimulatory action on LH secretion and a potentiation of the response of the gonadotrophes to LHRH. Thus the possibility exists that PACAP may enhance LH secretion not only by increased cAMP production but also by increasing cytosolic Ca2+ concentrations ([Ca2+]). In the present study we examined whether PACAP affects cytosolic [Ca2+] in identified rat gonadotrophes (as determined by the fura-method) and whether the suggested potentiating effect of PACAP on LHRH induced LH release is dependent on Ca2+. PACAP (1 nM) and 0.1 nM LHRH significantly increased LH concentrations in the culture medium after 5 hrs of incubation. Coincubation of cells with both peptides resulted in an additive increase of LH release. While the stimulatory effect LHRH was blunted in Ca(2+)-free medium, PACAP remained stimulatory to LH release. PACAP stimulated cAMP formation regardless whether the culture medium contained Ca2+ or not. Gonadotrophes were selected by their response to LHRH (1 microM) and were subsequently challenged with PACAP (1 microM). About 75% of gonadotrophes responded also to PACAP with an increase of cytosolic [Ca2+] which was blunted by removal of extracellular Ca2+. We suggest that in the rat pituitary the majority of the gonadotrophes are PACAP responsive as determined by an increase of cytosolic [Ca2+].(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 5","pages":"290-6"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211246","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19287436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 25
Elevated serum thyrotropin [TSH] levels in critically ill patients with acquired immunodeficiency syndrome (AIDS). 获得性免疫缺陷综合征(AIDS)危重患者血清促甲状腺素(TSH)水平升高
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211255
S A Peter, J M Ortiz, R Vergara
{"title":"Elevated serum thyrotropin [TSH] levels in critically ill patients with acquired immunodeficiency syndrome (AIDS).","authors":"S A Peter,&nbsp;J M Ortiz,&nbsp;R Vergara","doi":"10.1055/s-0029-1211255","DOIUrl":"https://doi.org/10.1055/s-0029-1211255","url":null,"abstract":"STUDY OBJECTIVE\u0000To determine thyrotropin (TSH) reserve in critically ill patients with Acquired Immunodeficiency Syndrome (AIDS).\u0000\u0000\u0000DESIGN\u0000Prospective longitudinal.\u0000\u0000\u0000SETTING\u0000Six hundred (600) bed municipal hospital serving a poor neighborhood in New York City with a high incidence of AIDS mainly from intravenous drug abuse.\u0000\u0000\u0000PATIENTS AND METHODS\u0000Twelve (12) patients with AIDS, who were in the Intensive Care Unit or critically ill on medical wards, were evaluated consecutively with baseline thyroid function tests and serum thyrotropin (TSH) response to thyroid releasing hormone testing.\u0000\u0000\u0000RESULTS\u000066.7% of patients had elevated TSH levels. All patients had low triiodothyronine (T3), six patients had low thyroxine (T4) levels.\u0000\u0000\u0000RESULTS\u0000(cont'd). Six patients met the criteria for hypothyroidism. Two patients met the criteria for subclinical hypothyroidism.\u0000\u0000\u0000CONCLUSION\u0000Elevated TSH levels and hypothyroidism are common in our critically ill population with AIDS.","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 6","pages":"346-9"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211255","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19149063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Structure of the POMC promoter region in pituitary and extrapituitary ACTH producing tumors. 垂体和垂体外促ACTH肿瘤中POMC启动子区的结构。
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211205
H Mönig, I U Ali, E H Oldfield, H M Schulte
{"title":"Structure of the POMC promoter region in pituitary and extrapituitary ACTH producing tumors.","authors":"H Mönig,&nbsp;I U Ali,&nbsp;E H Oldfield,&nbsp;H M Schulte","doi":"10.1055/s-0029-1211205","DOIUrl":"https://doi.org/10.1055/s-0029-1211205","url":null,"abstract":"<p><p>Proopiomelanocortin (POMC) is the common precursor of a variety of important endocrine peptides including ACTH. Transcription of the POMC gene is positively regulated by CRH through cAMP-responsive regions and is under negative feedback control by glucocorticoids which exert their inhibitory effect trough negative glucocorticoid responsive elements (nGRE). In vitro studies using the rat POMC promoter suggested that binding of the glucocorticoid receptor complex to a -63 bp binding site is correlated with repression of POMC gene transcription, and that specific mutations in this region abolish this effect. Impaired negative feedback regulation, though to a different degree, is a common feature of both corticotroph tumors (Cushing's disease) and extrapituitary ACTH producing tumors. We have analyzed the upstream promoter region of POMC gene from eleven patients with Cushing's disease, four of which had Nelson's syndrome, and from one patient with an ectopic ACTH syndrome secondary to a lung carcinoid for any possible mutations in the nGRE and/or cAMP-responsive sequences. DNA was purified from tumor tissue and was used as template for polymerase chain reaction (PCR). A segment between -371 and -19 bp of the POMC transcription start site was amplified and cloned into a plasmid vector. Sequencing was performed using the dideoxy chain termination procedure. Analysis of the 5'-flanking region revealed no defect in all tumors investigated. We conclude from our results that the defective glucocorticoid repression of POMC peptides production may be more likely due to aberrancies in other components of the complex transcriptional regulatory mechanism.</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 1","pages":"36-8"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211205","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19371545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Effects of selenium and iodine deficiency on type I, type II and type III iodothyronine deiodinases and circulating thyroid hormones in the rat. 硒和碘缺乏对大鼠I型、II型和III型碘甲状腺原氨酸脱碘酶和循环甲状腺激素的影响
Experimental and clinical endocrinology Pub Date : 1993-01-01 DOI: 10.1055/s-0029-1211212
H Meinhold, A Campos-Barros, B Walzog, R Köhler, F Müller, D Behne
{"title":"Effects of selenium and iodine deficiency on type I, type II and type III iodothyronine deiodinases and circulating thyroid hormones in the rat.","authors":"H Meinhold,&nbsp;A Campos-Barros,&nbsp;B Walzog,&nbsp;R Köhler,&nbsp;F Müller,&nbsp;D Behne","doi":"10.1055/s-0029-1211212","DOIUrl":"https://doi.org/10.1055/s-0029-1211212","url":null,"abstract":"<p><p>The effects of nutritional selenium (Se) deficiency over a period of three generations and of a combined selenium and iodine deficiency on hepatic and cerebrocortical iodothyronine deiodinases and on circulating thyroid hormone levels were examined in the rat. Se deficiency strongly decreased hepatic type I iodothyronine 5'- and 5-deiodinase to 6-13% of that in controls. Iodine depletion had only a marginal decreasing effect on the type I activity. Cerebrocortical type II 5'-deiodinase was decreased in Se-deficient, iodine-replete rats. Its 5-6-fold elevation in iodine-deficient rats was not reversed by additional selenium deficiency. Cortex type III 5-deiodinase was modestly decreased in all groups with insufficient trace element supply. Long-term Se deficiency has only limited effects on serum T4 and T3 levels. Two months of iodine deficiency decreased serum T4 to less than 10% of that in controls, but did not significantly affect serum T3 levels. The strong decrease of hepatic outer- and inner-ring deiodination of T4 in Se deficiency obviously reflects the reduced tissue concentration of the type I deiodinase which was recently identified as a selenoenzyme. The maintenance of increased cerebrocortical type II deiodinase in iodine-depleted animals irrespective of adequate or deficient selenium supply suggests that the type II isoenzyme does not contain selenium in its catalytic site. Further studies are necessary to clarify whether the weak, but repeatedly confirmed decrease of cortex type III deiodinase is the direct effect of Se deficiency or the indirect consequence of the multilevel change in thyroid hormone metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":12104,"journal":{"name":"Experimental and clinical endocrinology","volume":"101 2","pages":"87-93"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1055/s-0029-1211212","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19390459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 82
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