Hormone and Metabolic Research (HORM METAB RES)

Publisher: Georg Thieme Verlag

Journal description

Covering the fields of endocrinology and metabolism from both a clinical and basic science perspective, this well regarded monthly journal publishes original articles, and short communications on cutting edge topics. Speedy publication time is given high priority, ensuring that endocrinologists worldwide get timely, fast-breaking information as it happens.

Current impact factor: 2.12

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 2.121
2013 Impact Factor 2.038
2012 Impact Factor 2.145
2011 Impact Factor 2.188
2010 Impact Factor 2.414
2009 Impact Factor 2.686
2008 Impact Factor 2.715
2007 Impact Factor 2.254
2006 Impact Factor 1.997
2005 Impact Factor 2.049
2004 Impact Factor 1.946
2003 Impact Factor 1.669
2002 Impact Factor 1.608
2001 Impact Factor 1.91
2000 Impact Factor 1.707
1999 Impact Factor 1.465
1998 Impact Factor 2.242
1997 Impact Factor 1.152
1996 Impact Factor 0.89
1995 Impact Factor 0.674
1994 Impact Factor 0.735
1993 Impact Factor 0.585
1992 Impact Factor 0.721

Impact factor over time

Impact factor
Year

Additional details

5-year impact 1.99
Cited half-life 7.40
Immediacy index 0.50
Eigenfactor 0.01
Article influence 0.56
Website Hormone and Metabolic Research website
Other titles Hormone and metabolic research, Hormon- und Stoffwechselforschung, Hormones et métabolisme
ISSN 0018-5043
OCLC 1588475
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Georg Thieme Verlag

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Author's post-print or Publisher's version/PDF on author's personal website immediately
    • Author's post-print in Institutional Repository and PubMed Central after 12 months embargo
    • Publisher's version/PDF can be used on author's personal website only
    • Publisher copyright and source must be acknowledged
    • Link to Publisher version (www.thieme-connect.com) must be included if article has been published online
    • Publisher last contacted on 31/03/2015
    • 'Georg Thieme Verlag' is an imprint of 'Thieme Publishing'
  • Classification
    blue

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Patients with Xq26.3 microduplication present with X-linked acrogigantism (X-LAG) syndrome, an early-childhood form of gigantism due to marked growth hormone (GH) hypersecretion from mixed GH-PRL adenomas and hyperplasia. The microduplication includes GPR101, which is upregulated in patients' tumor tissue. The GPR101 gene codes for an orphan G protein coupled receptor that is normally highly expressed in the hypothalamus. Our aim was to determine whether GPR101 loss of function mutations or deletions could be involved in patients with congenital isolated GH deficiency (GHD). Taking advantage of the cohort of patients from the GENHYPOPIT network, we studied 41 patients with unexplained isolated GHD. All patients had Sanger sequencing of the GPR101 gene and array comparative genome hybridization (aCGH) to look for deletions. Functional studies (cell culture with GH secretion measurements, cAMP response) were performed. One novel GPR101 variant, c.589 G>T (p.V197L), was seen in the heterozygous state in a patient with isolated GHD. In silico analysis suggested that this variant could be deleterious. Functional studies did not show any significant difference in comparison with wild type for GH secretion and cAMP response. No truncating, frameshift, or small insertion-deletion (indel) GPR101 mutations were seen in the 41 patients. No deletion or other copy number variation at chromosome Xq26.3 was found on aCGH. We found a novel GPR101 variant of unknown significance, in a patient with isolated GH deficiency. Our study did not identify GPR101 abnormalities as a frequent cause of GH deficiency.
    No preview · Article · Jan 2016 · Hormone and Metabolic Research
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    ABSTRACT: The aim of this study was to determine serum soluble CD163 levels in patients with polycystic ovary syndrome and its relation to clinical and metabolic parameters. Eighty-four women aged 18-45 years, 43 with a polycystic ovary syndrome and 41 controls were recruited in this case-control study. Serum sCD163 levels of the goups were compared. Other metabolic, hormonal and clinical parameters including, body mass index, HOMA-IR, highly sensitive C- reactive protein, glucose, glycated hemoglobin, lipids, luteinizing hormone and total testosterone and waist/ hip circumference were also investigated. Patients were further subgrouped according to body mass index and sCD163 levels were investigated in obese and normal weight subjects. We performed a multiple regression analysis to investigate the independent predictors affecting soluble CD163 levels. Significantly higher soluble CD163 levels were found in patients with polycystic ovary syndrome (2.11±0.65 ng/ ml vs 1.69±0.85 ng/ml, p= 0.012). We detected positive correlations of sCD163 with total testosterone, total cholesterol and luteinizing hormone (r=0.330, p=0.002, r=0.356, p<0.001 and r=0.239, p=0.030 respectively). In the multiple lineer regression analysis, total testosterone was the variable associated with the elevation of serum soluble CD163 levels. Soluble CD163, which is identified as a marker of inflammation and type II diabetes, is elevated in polycystic ovary syndrome. Elevated sCD163 levels were found to be associated with total tetosterone. Further studies to elucidate the exact mechanism underlying the elevation of serum soluble CD163 in polycystic ovary syndrome are needed. Keywords: Soluble CD163, polycystic ovary syndrome, inflammation, obesity
    No preview · Article · Jan 2016 · Hormone and Metabolic Research
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    ABSTRACT: ATP-binding cassette transporter A1 (ABCA1) in pancreatic beta cells influences insulin secretion and cholesterol homeostasis. The present study investigates whether insulin-like growth factor 1 (IGF-1), which mediates stimulation of ABCA1 gene expression, could also interfere with the phosphatidylinositol 3-kinase (PI3-K) cascade.ABCA1 expression was examined by real-time polymerase chain reaction (PCR), Western blot analysis, and a reporter gene assay in rat insulin-secreting INS-1 cells incubated with IGF-1. The binding of forkhead box O1 (FoxO1) protein to the ABCA1 promoter was assessed by a chromatin immunoprecipitation (ChIP) assay. ABCA1 protein levels increased in response to rising concentrations of IGF-1. Real-time PCR analysis showed a significant increase in ABCA1 mRNA expression. However, both effects were suppressed after silencing the IGF-1 receptor. In parallel with its effect on endogenous ABCA1 mRNA levels, IGF-1 induced the activity of a reporter construct containing the ABCA1 promoter, while it was abrogated by LY294002, a specific inhibitor of PI3-K. Constitutively active Akt stimulated activity of the ABCA1 promoter, and a dominant-negative mutant of Akt or mutagenesis of the FoxO1 response element in the ABCA1 promoter abolished the ability of IGF-1 to stimulate promoter activity. A ChIP assay showed that FoxO1 mediated its transcriptional activity by directly binding to the ABCA1 promoter region. The knockdown of FoxO1 disrupted the effect of IGF-1 on ABCA1 expression. Furthermore, IGF-1 promoted cholesterol efflux and reduced the pancreatic lipotoxicity. These results demonstrate that the PI3-K/Akt/FoxO1 pathway contributes to the regulation of ABCA1 expression in response to IGF-1 stimulation.
    No preview · Article · Jan 2016 · Hormone and Metabolic Research
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    ABSTRACT: Several studies have shown an association between overt hypothyroidism and diastolic hypertension. Association between subclinical hypothyroidism and hypertension is a matter of debate. The aim of this study was to examine the association of systolic and diastolic blood pressure, pulse pressure and mean arterial blood pressure with serum thyroid hormones levels in euthyroid subjects.Data from 4 756 individuals of the Tehran Thyroid study (TTS) without any previously known thyroid disease were analyzed. We divided participants based on TSH tertiles. Serum TSH and free T4 (FT4) concentration, systolic blood pressure (SBP), diastolic blood pressure (BPD) body mass index (BMI) were measured in all subjects.Among 5 786 individuals participated, 4 985 were euthyroid. After implementing exclusion criteria, 4 756 individuals remained of whom 2 122 (44.6%) were male and 2 634 (55.4%) were female. Multiple linear regression analysis revealed no association between TSH levels within reference ranges and blood pressure profile. No significant relationship was observed between TSH levels and systolic or diastolic blood pressure or the mean arterial pressure or pulse pressure in each tertile of TSH. There was a negative association between pulse pressure and TSH in the second tertile (r=- 0.066, p=0.009). Regression analysis showed that FT4 was significantly associated with systolic blood pressure, diastolic blood pressure, pulse pressure and mean arterial pressure.No association was found between serum TSH and blood pressure profile in euthyroid subjects. Serum FT4 levels showed a positive association with blood pressure profiles.
    No preview · Article · Dec 2015 · Hormone and Metabolic Research
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    ABSTRACT: In recent years, an increasing number of studies have revealed deleterious effects of aldosterone via the mineralocorticoid receptor (MR). Especially in patients with primary aldosteronism (PA) a significant higher estimated risk of developing cardiovascular comorbidities and comortalities compared to essential hypertensives was reported. As diabetes mellitus and the metabolic syndrome are one of the major contributors to cardiovascular morbidity and mortality their connection to aldosterone excess became a focus of research in PA patients. Several studies assessed the effect of PA on glucose metabolism, the prevalence of diabetes mellitus, and the effect of PA treatment on both revealing different results. Therefore, we performed an extensive literature research. This review focuses on the current knowledge of the connection between aldosterone excess, glucose homeostasis, and diabetes mellitus in patients with PA. We have highlighted this topic from a pro and contra perspective followed by a summarizing concluding remark. Additionally, we have briefly reviewed the data on possible underlying mechanisms and indicated future considerations on the possible impact of cortisol co-secretion in PA.
    No preview · Article · Dec 2015 · Hormone and Metabolic Research

  • No preview · Article · Dec 2015 · Hormone and Metabolic Research
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    ABSTRACT: Primary aldosteronism (PA) is the most frequent cause of secondary arterial hypertension. Beyond its effects on intravascular volume and blood pressure, PA causes metabolic alterations and a higher cardiovascular morbidity, which is reduced by PA-directed therapy. Experimental studies demonstrated that mineralocorticoid excess may also influence mineral homeostasis. A role in cardiovascular disease has also been attributed to parathyroid hormone (PTH). Increasing evidence supports a bidirectional interaction between aldosterone and PTH. Primary hyperparathyroidism is associated with arterial hypertension and an increased cardiovascular morbidity and mortality, which might be associated to higher aldosterone values; parathyreoidectomy results in lowered aldosterone and blood pressure levels. PA leads to secondary hyperparathyroidism, which is reversible by PA-directed therapy. A lower bone mineral density and a higher fracture rate were also shown to be reversible by PA-directed therapy. There is a suspicion of a bidirectional interaction between aldosterone and PTH, which might lead to a higher cardiovascular risk. There are more and more reports about coincident PA and primary hyperparathyroidism. From a pathophysiologic point of view this constellation is best characterized as tertiary hyperparathyroidism. Future aspects should further clarify the extent of these endocrine interactions and analyze the influence of this interplay on cardiovascular morbidity and mortality and bone health.
    No preview · Article · Dec 2015 · Hormone and Metabolic Research
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    ABSTRACT: There have been 2, and possibly 3, major questions for primary aldosteronism (PA) answered at least in principle over the past 5 years. The first is that of somatic mutations underlying the majority of aldosterone producing adenomas. The second is the extension of our knowledge of the genetics of familial hypertension, and the third the role of renal intercalated cells in sodium homeostasis. New questions for the next 5 years include a single accepted confirmatory/exclusion test; standardisation of assays and cut-offs; alternatives to universal adrenal venous sampling; reclassification of 'low renin hypertension'; recognition of the extent of 'occult' PA; inclusion of low-dose mineralocorticoid receptor antagonist in first-line therapy for hypertension; and finally, possible resolution of the aldosterone/inappropriate sodium status enigma at the heart of the cardiovascular damage in PA.
    No preview · Article · Nov 2015 · Hormone and Metabolic Research
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    ABSTRACT: Increased risk of cerebrovascular accident in diabetes cannot be fully explained by traditional risk factors. Epidemiological studies show that postprandial hyperglycemia is strongly associated with cerebrovascular events and cerebrovascular-associated mortality. Postprandial hyperglycemia contributes to vascular damage by several mechanisms such as endothelial dysfunction, arthrosclerosis, oxidative stress, inflammation, and hypercoagulability. Hyperglycemia has deleterious effects on the vascular endothelium and leads to the development of cerebrovascular disease. Thus, an important strategy to reduce cerebrovascular risk in patients with diabetes is to reduce postprandial hyperglycemia. Glucagon-like peptide-1 receptor agonists, dipeptidyl peptidase-4 inhibitors, and α-glucosidase inhibitors predominantly reduce postprandial plasma glucose levels. Among all of these, α-glucosidase inhibitors reduces postprandial hyperglycemia by delaying carbohydrate absorption from the intestine and this mechanism provides glycemic control without exacerbating coexisting cerebrovascular risk factors. Good glycemic control is proven to reduce the risk of cardiovascular complications, but equivalent evidence for cerebrovascular risk reduction is lacking. This review examines the evidences that postprandial hyperglycemia plays a major role in vascular damage, along with the complex interplay between hyperglycemia and coexisting risk factors. Furthermore, the mechanism by which α-glucosidase inhibitors may prevent this vascular damage as well as risk of hypoglycemia with α-glucosidase inhibitors are examined. Thus, this review suggests that α-glucosidase inhibitors are useful in reducing the risk of cerebrovascular events in patients with diabetes.
    No preview · Article · Nov 2015 · Hormone and Metabolic Research
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    ABSTRACT: This study was performed to evaluate maternal thyroid dysfunction and autoimmunity during pregnancy and its correlation with thyroid function of offspring. In this cohort study, Serum TT4, TT3, T3U, TSH, TPOAb, and TgAb were measured. Serum samples of 120 pregnant women were collected during 3 trimesters as well as in 57 cord bloods, 69 neonates, 34, 37, and 36 infants aged 2, 4, and 6 months. Repeated measure and Pearson correlation test were used to compare thyroid hormone values and to assess the correlations, respectively. Main outcomes were correlations between thyroid hormones and antibodies in mothers and offspring. An increasing trend for TT3 (p for trend < 000.1) and TSH (p for trend 0.01) was found over the course of gestation. Among 120 mothers, 10 (8%) had subclinical hyperthyroidism and 18 mothers (15%) showed subclinical hypothyroidism. We found one hypothyroid (0.8%) and 3 hyperthyroid (2.5%) mothers during pregnancy. Correlations among maternal thyroid hormones were found but not with auto-antibodies. A positive correlation between maternal thyroid auto-antibodies in all trimesters with cord blood and neonates was found. Cord blood TSH had a good correlation with maternal TSH, but only in the first trimester (r=0.29, p<0.05). A positive correlation between neonatal TSH and maternal TT4 was found only in the third trimester (r=0.25, p<0.05). Subclinical hypothyroidism was the most common thyroid dysfunction in the pregnant women studied. The association between maternal auto-antibodies and thyroid hormones of offspring was observed mostly in the neonatal period and became weaker after one month of age.
    No preview · Article · Nov 2015 · Hormone and Metabolic Research
  • J Lv · Y Pan · X Li · D Cheng · H Ju · J Tian · H Shi · Y Zhang
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    ABSTRACT: Irisin is a newly discovered factor that is secreted by skeletal muscle and plays an important role in the homeostasis and metabolism of energy balance. This study used irisin radiolabeled with (125)I and small-animal SPECT/CT imaging to investigate the metabolic elimination and distribution of irisin in vivo. Irisin was labeled with (125)I using the Iodogen method. Small-animal SPECT/CT imaging was performed on C57/B16 mice at 15, 30, 60, 120, and 240 min after receiving a tail vein injection, and the radioactive distribution in the organs of mice was determined at 15, 60, and 120 min. Small-animal SPECT/CT imaging revealed the highest level of radioactivity in the gallbladder followed by the liver and kidney. Radioactivity decreased gradually with time in all organs. The radioactive distribution in the mice organs also showed that the highest %ID/g was in the gallbladder followed by the kidney and liver, and decreased gradually with time. The radioactivity in the gastric system reached its highest level at 60 min. Finally, our study showed the metabolic clearance of (125)I-irisin is achieved primarily through the hepatobiliary and renal system and provided the basis for the clinical application of irisin. © Georg Thieme Verlag KG Stuttgart · New York.
    No preview · Article · Mar 2015 · Hormone and Metabolic Research
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    ABSTRACT: The functions of hypothalamic-pituitary-thyroid axis are attenuated in type 1 diabetes mellitus due to insulin deficiency. The use of intranasally administered insulin is of considerable interest for treatment of diabetes and cognitive disorders, but its effect on the thyroid system has not been investigated yet. We studied the influence of long-term treatment with intranasal insulin on the hypothalamic-pituitary-thyroid axis of nondiabetic rats and diabetic animals with streptozotocin models of acute and mild type 1 diabetes mellitus. This treatment was carried out for 28 days in acute (daily does of 0.3, 0.6, and 1.5 IU of insulin per rat) and for 135 days in mild diabetes (daily dose of 0.45 IU/rat). Nondiabetic rats were treated in a similar manner. Intranasal insulin in both models of diabetes resulted in the improvement of thyroid status; manifested as increase of thyroid hormones levels and restoration of response to thyroliberin. In acute diabetes, a daily dose of 0.6 IU/rat was the most effective. Twenty eight days treatment of nondiabetic rats with intranasal insulin at a dose of 0.3 IU/rat resulted in a significant increase of free and total thyroxine levels. Longer treatment of rats with mild diabetes and nondiabetic animals significantly increased thyrotropin level. Thus, long-term intranasal insulin treatment restored the hypothalamic-pituitary-thyroid axis function in type 1 diabetes, but led to a significant increase in the thyrotropin level, which must be considered when designing a strategy for the use of intranasal insulin in clinical applications. © Georg Thieme Verlag KG Stuttgart · New York.
    No preview · Article · Mar 2015 · Hormone and Metabolic Research
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    ABSTRACT: A decade has passed since the Chicago Consensus meeting was convened to consider how to improve the management of individuals and their families with an intersex disorder. It is apposite to review, from an individual perspective, what impact the Consensus has had on clinical practice and research. Emphasis is placed on nomenclature and DSD classification, multidisciplinary team working, striving to reach a causative diagnosis for DSD, the value of uniformity of collective case registries for rare conditions, and the potential for meaningful clinical outcome studies and basic scientific research. The impact of the Consensus can be gauged objectively by an exponential increase in DSD-related publications in the medical and scientific literature and organisation of numerous national and international meetings. Psychologists and social scientists have embraced the subject area and enhanced the holistic approach to management of DSD. Much needs to be done to improve diagnosis, and to identify measures to predict outcome that can be used both in sex assignment decision-making and to improve the quality of life for young adults with DSD. Though challenging, these goals are attainable through specialist multidisciplinary clinics working at local level and the DSD community at large, collaborating at national and international levels to tap the data resources now being developed. © Georg Thieme Verlag KG Stuttgart · New York.
    No preview · Article · Mar 2015 · Hormone and Metabolic Research
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    ABSTRACT: The objective of the study was to evaluate the roles of central and peripheral T3 regulation. In a prospective study involving 1 796 patients, the equilibria between FT3 and TSH were compared in untreated and L-T4-treated patients with varying functional states, residual thyroid secretory capacities and magnitudes of TSH stimulation. T3 concentrations were stable over wide variations in TSH levels (from 0.2 to 7 mU/l) and endogenous T4 production in untreated patients, but unbalanced in L-T4-treated athyreotic patients where T3 correlated with exogenous T4 supply. T3 stability was related to TSH-stimulated deiodinase activity by clinical observation, as predicted by theoretical modelling. Deiodinase activity in treated patients was reduced due to both diminished responsiveness to TSH and lack of thyroidal capacity. Deiodinase activity was increased in high thyroid volume, compared to lower volumes in euthyroid patients (<5 ml, p<0.001). While deiodinase differed between euthyroid and subclinically hypothyroid patients in high volume, 26.7 nmol/s (23.6, 29.2), n=214 vs. 28.9 nmol/s (26.7, 31.5), n=20, p=0.02, it was equivalent between the 2 functional groups in low volume, 23.3 nmol/s (21.3, 26.1), n=117 vs. 24.6 nmol/s (22.2, 27.5), n=38, p=0.22. These findings suggest that the thyroid gland and peripheral tissues are integrated in the physiological process of T3 homeostasis in humans via a feed-forward TSH motif, which coordinates peripheral and central regulatory mechanisms. Regulatory and capacity deficiencies collectively impair T3 homeostasis in L-T4-treated patients. © Georg Thieme Verlag KG Stuttgart · New York.
    No preview · Article · Mar 2015 · Hormone and Metabolic Research