Hormone research最新文献

{"title":"Ghrelin and new metabolic frontiers.","authors":"Aart Jan van der Lely","doi":"10.1159/000178055","DOIUrl":"https://doi.org/10.1159/000178055","url":null,"abstract":"<p><strong>Background: </strong>A growing body of literature has profiled the complex identities and interactions of ghrelin analogues and their known and unknown receptors, which constitute the ghrelin system. In humans, acylated ghrelin (AG) induces a rapid rise in glucose and insulin levels. However, coadministration of unacylated ghrelin (UAG) counteracts this effect. Accumulating data support the existence of a specific receptor for UAG in addition to the corticotropin-releasing factor 2 receptor and the growth hormone secretagogue type 1a receptor. Preclinically, mice that overexpress UAG exhibit decreased body weight, food intake, free fatty acid levels and fat pad mass weight and moderately decreased linear growth. In humans, intravenous infusion of UAG in normal subjects enhances the early insulin response to meals, improves glucose metabolism and insulin sensitivity and inhibits lipolysis.</p><p><strong>Conclusions: </strong>AG and UAG play an important regulatory role in metabolism.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 1 ","pages":"129-33"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000178055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27932031","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}

{"title":"Bone and metabolism: a complex crosstalk.","authors":"Liesbet Lieben,&nbsp;Filip Callewaert,&nbsp;Roger Bouillon","doi":"10.1159/000178056","DOIUrl":"https://doi.org/10.1159/000178056","url":null,"abstract":"<p><strong>Background: </strong>Until recently, communication from metabolism to bone was considered purely unidirectional, involving complex interactions among an adipocyte-derived factor (leptin), the sympathetic nervous system and neuropeptides. However, studies in animal models now show that bone regulates glucose metabolism and fat mass via the uncarboxylated form of an osteoblast-derived factor (osteocalcin). These findings not only demonstrate that energy metabolism regulates bone remodeling through neural relays, but also that the skeleton acts as an endocrine tissue that regulates metabolic homeostasis.</p><p><strong>Conclusions: </strong>Further study is needed to understand the physiological role of these complex interactions in man and their implications for human diseases.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 1 ","pages":"134-8"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000178056","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27932032","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}

{"title":"Pitfalls of insulin-like growth factor I assays.","authors":"Martin Bidlingmaier","doi":"10.1159/000178034","DOIUrl":"https://doi.org/10.1159/000178034","url":null,"abstract":"<p><strong>Background: </strong>Immunoassays that measure circulating concentrations of insulin-like growth factor I (IGF-I) are increasingly used to diagnose and monitor growth hormone (GH)-related diseases. Specifically, IGF-I measured by immunoassay is used to diagnose GH deficiency and acromegaly, and to monitor treatment efficacy in patients with acromegaly, particularly those treated with the GH receptor antagonist pegvisomant, as measurement of circulating GH is no longer suitable for monitoring disease activity. While techniques for measuring IGF-I have evolved over the decades, immunoassays are still the primary tool used in routine laboratories. Immunoassays depend on the interaction between antibodies and the analyte, and all factors that modify the accessibility of the epitopes recognized by the antibodies can influence results. With IGF-I assays, interference from binding proteins is an important variable affecting assay results.</p><p><strong>Conclusions: </strong>It is generally accepted that assay- and age-specific reference ranges are mandatory for meaningful interpretation of IGF-I concentrations. High-quality, method-specific reference ranges and a high degree of methodological consistency in the assay are essential for reliable comparison of results across studies and for long-term monitoring of individual patients.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 1 ","pages":"30-3"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000178034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27932282","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}

{"title":"Update on familial pituitary tumors: from multiple endocrine neoplasia type 1 to familial isolated pituitary adenoma.","authors":"Adrian F Daly,&nbsp;Maria A Tichomirowa,&nbsp;Maria A Tichomirow,&nbsp;Albert Beckers","doi":"10.1159/000178050","DOIUrl":"https://doi.org/10.1159/000178050","url":null,"abstract":"<p><strong>Background: </strong>Pituitary adenomas occur in a familial setting in about 5% of all cases and over half of these are due to multiple endocrine neoplasia type 1 (MEN1) and Carney complex (CNC). Since the late 1990s, we have described non-MEN1/CNC familial pituitary tumors that include all tumor phenotypes and have named this condition 'familial isolated pituitary adenoma' (FIPA). Clinical features of FIPA differ from those of sporadic pituitary adenomas in that patients with FIPA are often younger and have larger tumors at diagnosis. About 15% of FIPA patients have mutations in the aryl hydrocarbon receptor interacting protein gene (AIP), which indicates that FIPA may have a diverse genetic pathophysiology. We review the clinical features of FIPA, the tumor pathologies found in this setting and the genetic/molecular data that have been recently reported.</p><p><strong>Conclusions: </strong>Clinically relevant pituitary adenomas are more common than previously thought and occur in a familial setting in about 5% of cases overall. Therefore, specific questioning regarding family history of pituitary disease should be part of the workup of all patients with pituitary adenomas, not just those with acromegaly. FIPA is a useful clinical framework to study the features of pituitary adenomas that occur in a familial setting since it encompasses all tumor phenotypes and heterogeneous/homogeneous expression among affected family members.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 1 ","pages":"105-11"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000178050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27933130","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}

{"title":"Isolated lymphocytic infiltration of pituitary stalk preceding the diagnosis of germinoma in 2 prepubertal children treated with growth hormone.","authors":"T Edouard,&nbsp;D E J Stafford,&nbsp;I Oliver,&nbsp;M Jesuran,&nbsp;A I Bertozzi,&nbsp;C Cances,&nbsp;S Boetto,&nbsp;C Guilbeau-Frugier,&nbsp;B Delisle,&nbsp;M Tauber","doi":"10.1159/000224342","DOIUrl":"https://doi.org/10.1159/000224342","url":null,"abstract":"<p><p>We report the clinical course of 2 patients with central diabetes insipidus and evolving to panyhypopituitarism which prompted the diagnosis of an isolated pituitary stalk thickening (PST). In both patients, all etiological investigations were normal and the first biopsy revealed an isolated lymphocytic infiltrate with no sign of malignancy. Close clinical follow-up accompanied by serial brain MRIs was proposed to determine a precise diagnosis and for early detection and treatment of neoplastic disease. In our first case, the diagnosis of germinoma was made 9 months after the PST diagnosis owing to tumor progression. In the second case, the time course was even longer with the diagnosis of germinoma 6 years following initial presentation. In these cases, it is speculated that the lymphocytic infiltrates represent the first sign of a host reaction to an occult germinoma. To our knowledge, this is the third case reported of lymphocytic infiltrates preceding a germinoma in a prepubertal girl, and the only case reported in a prepubertal boy. These cases underline the difficulties in establishing the diagnosis of germinoma in a patient with isolated PST.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"72 1","pages":"57-62"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000224342","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28357737","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}

{"title":"A favorable metabolic and antiatherogenic profile in carriers of CYP21A2 gene mutations supports the theory of a survival advantage in this population.","authors":"Sarantis Livadas,&nbsp;Maria Dracopoulou,&nbsp;Christina Lazaropoulou,&nbsp;Ioannis Papassotiriou,&nbsp;Amalia Sertedaki,&nbsp;G Nick Angelopoulos,&nbsp;George P Chrousos,&nbsp;Catherine Dacou-Voutetakis","doi":"10.1159/000249161","DOIUrl":"https://doi.org/10.1159/000249161","url":null,"abstract":"<p><strong>Context: </strong>The very high carrier frequency of 21-hydroxylase deficiency worldwide has been postulated as indicating a survival advantage. The 'mediators' of such an effect remain speculative.</p><p><strong>Objective: </strong>To look for possible differences in the metabolic and atherogenic risk profile of carriers and noncarriers of CYP21A2 gene mutations at puberty in order to identify possible mediators of the presumed survival advantage for the carriers. It is anticipated that by studying atherogenic risk factors at such an early developmental stage, age-related alterations in these factors may be minimized.</p><p><strong>Methods: </strong>The study group included 45 adolescent girls diagnosed in our center with premature pubarche, 29 of whom were noncarriers and 16 carriers of CYP21A2 mutations. The two groups did not differ in chronological age, age at pubarche or menarche, pubertal stage, body mass index and waist-to-hip ratio. Biochemical and hormonal profile markers as well as markers of endothelial dysfunction were determined by appropriate methodology. Additionally, in each subject, an oral glucose tolerance test and a gonadotrophin-releasing hormone GnRH analogue stimulation test were carried out.</p><p><strong>Results: </strong>Endothelin-1 values were lower in the carriers compared to the noncarriers (p = 0.031). Higher tissue plasminogen activator and lower plasminogen activator inhibitor-1 values were found in carriers compared to noncarriers (p = 0.02 and <0.001, respectively). The ratio of the insulinogenic index/homeostasis model assessment for insulin resistance, which reflects beta-cell function, was higher in carriers (p = 0.048), indicating a more favorable beta-cell function in the carriers.</p><p><strong>Conclusions: </strong>Our findings that carriers of CYP21A2 gene mutations have a more favorable internal milieu with regard to the metabolic syndrome and atherogenesis support the theory that heterozygous CYP21A2 mutations provide a survival advantage. The mechanisms involved may be related to the insulin secretion-action pathway, hypothalamic-pituitary-adrenal axis responsiveness or other still unrecognized factors.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"72 6","pages":"337-43"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000249161","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28448222","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}

{"title":"Metformin, estrogen replacement therapy and gonadotropin inhibition fail to improve insulin sensitivity in a girl with aromatase deficiency.","authors":"Gabriela Guercio,&nbsp;Maria Isabel Di Palma,&nbsp;Carolina Pepe,&nbsp;Nora I Saraco,&nbsp;Mariana Prieto,&nbsp;Carola Saure,&nbsp;Carmen Mazza,&nbsp;Marco A Rivarola,&nbsp;Alicia Belgorosky","doi":"10.1159/000249165","DOIUrl":"https://doi.org/10.1159/000249165","url":null,"abstract":"<p><strong>Background: </strong>Insulin resistance (IR), abnormal lipid profile, and other features of the metabolic syndrome have been described in CYP19 gene knockout mice and in aromatase-deficient adult men but not in prepubertal affected girls.</p><p><strong>Aims: </strong>To study insulin sensitivity, as well as the effects of estrogen, metformin and GnRHa treatment on glucose homeostasis, in an aromatase-deficient girl.</p><p><strong>Methods: </strong>Clinical, metabolic and hormonal follow-up data, from 8 to 12 years of age, is presented.</p><p><strong>Results: </strong>At 9 years of age, IR (HOMA 5.6) and glucose intolerance was detected, along with high serum testosterone (2.28 nmol/l), androstenedione (4.92 nmol/l) and FSH (13.4 mIU/ml) levels. Estrogen replacement was ineffective to suppress gonadotropin and androgen levels, as well as IR. Under metformin therapy, she developed type 2 diabetes and acanthosis nigricans. GnRHa administration for 1 year resulted in marked decreases in gonadotropin and serum androgens, but severe IR persisted.</p><p><strong>Conclusion: </strong>Postnatal estrogen replacement and a marked decrease of endogenous androgens failed to improve IR and glucose tolerance. We propose that, in females, the increment of androgens and/or lack of estrogens during fetal life might alter the mechanism of fetal programming of insulin sensitivity.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"72 6","pages":"370-6"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000249165","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28450402","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}

{"title":"Abnormal responses to TRH in children born small for gestational age that failed to catch up.","authors":"Ana Keselman,&nbsp;Ana Chiesa,&nbsp;Saúl Malozowski,&nbsp;Ana Vieytes,&nbsp;Juan Jorge Heinrich,&nbsp;Laura Gruñeiro de Papendieck","doi":"10.1159/000232492","DOIUrl":"https://doi.org/10.1159/000232492","url":null,"abstract":"<p><strong>Background: </strong>Fifteen percent of small for gestational age (SGA) children remain short and undergo thyroid axis evaluations.</p><p><strong>Methods: </strong>We analyzed data on thyroid assessment of 58 SGA children. Five had primary autoimmune hypothyroidism. In the remaining 53 patients, TSH, free T4 (FT4), antithyroid antibodies and 90-min TRH test results were analyzed. Patients were grouped into G1 (n = 27; normal) and G2 (n = 26; abnormal) according to their response to the TRH test compared with 30 normal children.</p><p><strong>Results: </strong>No differences were found in chronological age, gestational age, or birth weight standard deviation score (SDS) between groups. G2 showed higher SDS BMI at consultation (p < 0.05). FT4 (ng/dl) levels were similar in all groups, while basal TSH levels were statistically different in G2 compared with G1 and controls. In 21 G2 patients treated with thyroxine, FT4 levels did not change, TSH normalized, BMI SDS and height remained unchanged.</p><p><strong>Conclusion: </strong>These data suggest that in SGA short children thyroid abnormalities may occur. Some of them may be due to a different setting of the hypothalamic-hypophyseal-thyroid axis during intrauterine life. Intrauterine growth retardation may permanently influence endocrine systems by affecting their programming during development. Further follow-up is needed to confirm these findings and to assess their natural history and potential clinical impact.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"72 3","pages":"167-71"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000232492","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28458145","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}

{"title":"Plant growth regulator (4-chlorophenoxy acetic acid) increases apoptosis in gonads of rats without changing hormonal levels.","authors":"Ediz Yeşilkaya,&nbsp;Aysun Bideci,&nbsp;Ciğdem Ozer,&nbsp;Ciğdem Elmas,&nbsp;Orhun Camurdan,&nbsp;Seren Gulsen Giray,&nbsp;Mehmet Boyraz,&nbsp;Sebahattin Vurucu,&nbsp;Peyami Cinaz","doi":"10.1159/000236084","DOIUrl":"https://doi.org/10.1159/000236084","url":null,"abstract":"<p><strong>Background/aims: </strong>Plant growth regulators are considered to leave minimal amounts of remnants and therefore cause no significant side effects in humans. In this study, we aimed to investigate the hormonal and histopathological effects of 4-chlorophenoxy acetic acid (4-CPA), a commonly used plant growth regulator, on the gonadal functions of rats.</p><p><strong>Methods: </strong>The study was implemented on 64 Wistar albino rats (20 days old). Forty-eight rats received 4-CPA every day until 50 days of age. The rats were randomized into 4 groups (a control group and three 4-CPA groups with doses of 25, 50 and 100 mg/kg/day); each group was further divided into males and females, making a total of 8 groups. The levels of FSH, LH, testosterone, estradiol, leptin, inhibin-B and neuropeptide-Y were measured. Histopathological examination of the testes and ductus deferens in male rats, and ovaries and uterus of female rats (caspase-3 and -9 immunoreactivity) was performed.</p><p><strong>Results: </strong>Although hormone levels were similar between the groups, rats that received 4-CPA showed significantly higher degrees of apoptosis compared to the control group (p < 0.001) and increased doses of 4-CPA were directly correlated with the amount of apoptosis (p < 0.001).</p><p><strong>Conclusion: </strong>4-CPA induced apoptosis in the gonads of rats without concurrent changes in plasma hormone levels.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"72 4","pages":"225-35"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000236084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40040532","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}

{"title":"Treatment of growth hormone deficiency in adults.","authors":"Gudmundur Johannsson","doi":"10.1159/000178052","DOIUrl":"https://doi.org/10.1159/000178052","url":null,"abstract":"<p><strong>Background: </strong>The Growth Hormone Research Society held a Consensus Workshop in Sydney, Australia, in March 2007 to review advances in the management of growth hormone (GH) deficiency in adults and to update consensus recommendations.</p><p><strong>Objective: </strong>This short review summarizes key background information presented at the workshop and the consensus recommendations that followed.</p><p><strong>Conclusions: </strong>The benefits of GH replacement in GH-deficient adults are evident throughout life. Clinical response to treatment should be assessed by monitoring biochemistry values, body composition and quality of life. There is no evidence that GH replacement increases the risk of tumour recurrence or de novo malignancy.</p>","PeriodicalId":13225,"journal":{"name":"Hormone research","volume":"71 Suppl 1 ","pages":"116-22"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000178052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27933132","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}