Hormone and Metabolic Research Journal Impact Factor & Information

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

2015 Impact Factor Available summer 2016
2014 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

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

Publications in this journal

  • [Show abstract] [Hide abstract]
    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.
    Hormone and Metabolic Research 11/2015; DOI:10.1055/s-0035-1565182
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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.
    Hormone and Metabolic Research 11/2015; DOI:10.1055/s-0035-1565181
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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.
    Hormone and Metabolic Research 11/2015; DOI:10.1055/s-0035-1555878
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    ABSTRACT: Somatic mutations have been identified in the KCNJ5 gene (encoding the potassium channel GIRK4) in aldosterone-producing adenomas (APA). Most of these mutations are located in or near the selectivity filter of the GIRK4 channel pore and several have been shown to lead to the constitutive overproduction of aldosterone. KCNJ5 mutations in APA are more frequent in women; however, this gender dimorphism is a reported phenomenon of Western but not East Asian populations. In this review we discuss some of the issues that could potentially underlie this observation.
    Hormone and Metabolic Research 11/2015; DOI:10.1055/s-0035-1565090
  • 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.
    Hormone and Metabolic Research 03/2015; 47(08). DOI:10.1055/s-0035-1547261
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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.
    Hormone and Metabolic Research 03/2015; 47(05). DOI:10.1055/s-0035-1545274
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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.
    Hormone and Metabolic Research 03/2015; 47(12). DOI:10.1055/s-0035-1547236
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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.
    Hormone and Metabolic Research 03/2015; DOI:10.1055/s-0034-1398616
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    ABSTRACT: Children with chronic illnesses face multiple challenges as they mature into adulthood, which relate to independence, access to care, and changes in care providers. The scope and magnitude of these problems is amplified in children with disorders of sex development (DSD). In these children, the normal progression of pubertal events can be early, late, contrasexual, pharmacologically assisted, or some combination of these features. The diagnosis of DSD can occur in childhood, which gives the family some time to prepare for future events, but in other cases, the diagnosis is made during adolescence as the condition becomes apparent. This article discusses the difficulties these children and their families face during adolescence, provides an overview of the transitioning process, and uses a few conditions as examples to illustrate particular aspects. © Georg Thieme Verlag KG Stuttgart · New York.
    Hormone and Metabolic Research 03/2015; 47(05). DOI:10.1055/s-0035-1545303
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    ABSTRACT: The aim of this study was to investigate atherosclerotic risk markers in women with clinically nonfunctioning pituitary adenomas (CNFAs). Records of 47 women with CNFAs and 73 healthy women who were treated as outpatients between January 2010 and March 2014 were evaluated retrospectively. All study data were obtained from file records. Lipid parameters, mean platelet volume (MPV), total testosterone (TT), androstenedione (AS), and dehydroepiandrostenedione sulfate (DHEAS) were recorded. Insulin resistance (IR) was calculated with homeostatic model assessment-insulin resistance (HOMA-IR). Among the atherosclerotic risk markers, the HOMA-IR and AS levels were higher in patients with CNFAs than in healthy subjects (p=0.003, p=0.021, respectively). A positive correlation between AS and insulin/HOMA-IR levels was found among the metabolic parameters in the patients with CNFAs (p=0.001, r=0.550, p=0.004, r=0.498, respectively). The data showed that patients with CNFAs had high atherosclerotic risk markers such as insulin resistance and hyperandrogenemia. Insulin resistance may also cause hyperandrogenemia in patients with CNFAs. © Georg Thieme Verlag KG Stuttgart · New York.
    Hormone and Metabolic Research 03/2015; 47(9). DOI:10.1055/s-0035-1547234
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    ABSTRACT: Morbidity from adrenal insufficiency (AI) in Australia is poorly described. The objective of this study was to evaluate AI morbidity patterns in adults between 1999/2000 and 2011/2012 using national databases. A descriptive study of hospitalisations for AI and adrenal crises (AC) in adults and trends in prescriptions for 2 short-acting glucocorticoids (GC) was designed. The setting was the Australian healthcare system. Main outcome measures are the trends in hospitalisation and prescription rates. There were 7 378 hospital admissions for treatment of AI in adults between 1999/00 and 2011/12. Of these, 29.5% were for an AC. Admission rates for AC increased from 9.5 to 12.4 admissions/10(6)/year (p<0.05). There was a 5.8% decrease in admission rates for AI (excluding AC), from 27.0 to 25.5/10(6)/year (p=ns). Short-acting GC [hydrocortisone (HCT) and cortisone acetate (CA)] prescription rates increased significantly (p<0.001) from 3 176.1/10(6) to 3 463.8/10(6). Prescription rates for CA decreased by 22.4% (p<0.001) but HCT prescription rates increased to 77.1% (p<0.001). The increase in AC admission rates was positively correlated with the rise in both the total GC prescription rate (r=0.63, p<0.05) and the HCT prescription rate (r=0.74, p<0.01). Over the 13-year study period, there was a 30.8% increase in hospitalisation rates for ACs and a concomitant 77.1% increase in prescribing of HCT. The association between AC events and HCT use and/or reduced effective GC dose is plausibly causal, but confirmatory studies are required before suggesting any change to GC replacement in AI. © Georg Thieme Verlag KG Stuttgart · New York.
    Hormone and Metabolic Research 03/2015; 47(06). DOI:10.1055/s-0034-1395680
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    ABSTRACT: The syndrome of resistance to thyroid hormone (RTH β) is an inherited disorder characterized by variable tissue hyposensitivity to 3,5,30-l-triiodothyronine (T3), with persistent elevation of free-circulating T3 (FT3) and free thyroxine (FT4) levels in association with nonsuppressed serum thyrotropin (TSH). Clinical presentation is variable and the molecular analysis of THRB gene provides a short cut diagnosis. Here, we describe 2 cases in which RTH β was suspected on the basis of laboratory findings. The diagnosis was confirmed by direct THRB sequencing that revealed 2 novel mutations: the heterozygous p.Ala317Ser in subject 1 and the heterozygous p.Arg438Pro in subject 2. Both mutations were shown to be deleterious by SIFT, PolyPhen, and Align GV-GD predictive methods. © Georg Thieme Verlag KG Stuttgart · New York.
    Hormone and Metabolic Research 03/2015; 47(12). DOI:10.1055/s-0035-1545305
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    ABSTRACT: The short-term responses of gut hormones and the compensative interaction during a one-week period after subtotal gastrectomy in early gastric cancer (EGC) patients were assessed. Previous studies have reported gut hormonal changes after Roux-en-Y gastric bypass surgery. Blood samples were collected from 40 patients with EGC preoperatively, at 1 h after gastric resection, and on postoperative day (POD) 1, 3, and 7. Levels of active ghrelin, total ghrelin, obestatin, and PYY3-36 were measured. Total ghrelin level rapidly reached a nadir of 69.1%, while active ghrelin level had increased to 135.5% at 1 h after resection. Then, both returned to preoperative level. On the contrary, active/total ghrelin reached its nadir quickly at 1 h after resection and had returned to the preoperative level by POD 3. The nadir PYY3-36 level was 71.4% on POD 1, followed by a gradual recovery, and had increased to 116.5% by POD 7. The same pattern was observed for obestatin. Active ghrelin/obestatin showed an increase on POD 1 while total ghrelin/obestatin showed a decrease on POD 3. Then, both returned to preoperative level. These results suggest that a rapid interactive compensatory mechanism of gut hormones does exist in the remnant gastrointestinal tract after abrupt changes in the production reservoir in nonobese people. © Georg Thieme Verlag KG Stuttgart · New York.
    Hormone and Metabolic Research 02/2015; 47(04). DOI:10.1055/s-0034-1398663