Hormone and Metabolic Research (HORM METAB RES )

Publisher: Georg Thieme Verlag

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.

  • Impact factor
    2.15
    Show impact factor history
     
    Impact factor
  • 5-year impact
    2.17
  • Cited half-life
    7.00
  • Immediacy index
    0.77
  • Eigenfactor
    0.01
  • Article influence
    0.59
  • 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
    • On author's personal website immediately
    • On 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
    • 'Georg Thieme Verlag' is an imprint of 'Thieme Publishing'
  • Classification
    ​ blue

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Short-term abstinence from food intake, planned or unplanned, is unavoidable in modern life, but negatively correlated with appetite control and obesity. This study investigated the role of estradiol in feeding and body weight (BW) reactions to short-span cessation of feeding. During acute 1-6-h re-feeding, 12-h food-deprived (FD), estradiol benzoate (EB)-implanted ovariectomized rats ate less food and gained less weight than FD animals implanted with oil (O). Full fed (FF)- and FD-EB consumed equal amounts of food over 24 h, but weight gain was greater in the latter; 24-h food intake and BW gain in FD-O exceeded FD-EB. Caudal fourth ventricular administration of the AMPK activator AICAR increased dorsal vagal complex AMPK activity in FD-EB and FD-O, but elicited dissimilar adjustments in hypothalamic metabolic neuropeptide transmitter expression, while respectively enhancing or reducing acute re-feeding in these animals and reversing FD-O weight gain. Drug-treated FD-EB and FD-O exhibited respective feeding and weight gain increases between 6-24 h. AICAR enhanced 24-h consumption in FD-EB vs. FF-EB, but cumulative intake and BW gain were greater in AICAR-treated FD-O vs. FD-EB. Results show that estradiol limits acute re-feeding after short-term feeding suspension, but augments acute re-feeding when energy depletion coincides with suspended feeding. This compound metabolic stress exerts steroid-dependent effects during later resumption of circadian-induced feeding, for example, increased consumption vs. weight gain in the presence vs. absence of estradiol. These studies provide novel evidence that estrogen mitigates acute and post-acute adverse effects of disrupted fuel acquisition on energy balance.
    Hormone and Metabolic Research 09/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Previous studies have shown that in diabetes mellitus, insulin-induced relaxation of arteries is impaired and the level of ortho-tyrosine (o-Tyr), an oxidized amino acid is increased. Thus, we hypothesized that elevated vascular level of o-Tyr contributes to the impairment of insulin-induced vascular relaxation. Rats were fed with o-Tyr for 4 weeks. Insulin-induced vasomotor responses of isolated femoral artery were studied using wire myography. Vascular o-Tyr content was measured by HPLC, whereas immunoblot analyses were preformed to detect eNOS phosphorylation. Sustained oral supplementation of rats with o-Tyr increased the content of o-Tyr in the arterial wall and significantly reduced the relaxations to insulin. Sustained supplementation of cultured endothelial cells with o-Tyr increased the incorporation of o-Tyr and mitigated eNOS Ser (1 177) phosphorylation to insulin. Increasing arterial wall o-Tyr level attenuates insulin-induced relaxation - at least in part - by decreasing eNOS activation. Elevated level of o-Tyr could be an underlying mechanism for vasomotor dysfunction in diabetes mellitus.
    Hormone and Metabolic Research 09/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Recently, hypothalamic RFRP-3 (a mammalian ortholog of avian GnIH) signaling has been proposed as an important negative modulator of the reproductive axis. The current study examined whether repression of reproductive hormonal expression during short-term fasting conditions in higher-order primate is influenced by altered RFRP-3 signaling. Eight intact postpubertal male macaques (Macaca mulatta) were administered a single intravenous bolus of RF-9 (n=4), a potent and putative RFRP-3 receptor antagonist, or vehicle (n=4) following a 48-h fasting condition. Intermittent blood samples were collected every 30 min during the 4-h post-bolus period, and blood glucose, plasma cortisol, and testosterone concentrations were measured. Relative to fed conditions, fasting reduced glucose and testosterone levels (p<0.005) and increased cortisol levels (p<0.05). Relative to baseline, mean testosterone levels were elevated 150 min after RF-9 (p<0.05) but not vehicle administration. In addition, elevated mean plasma testosterone levels following RF-9 administration were equivalent to levels observed in normal fed monkeys. These results suggest an important role for RFRP-3 signaling in conveying metabolic state information to the reproductive axis in higher primates.
    Hormone and Metabolic Research 09/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hypothyroidism is a relatively common endocrine disorder usually accompanied with changes in serum lipid profiles. The purpose of this study was to assess the association between dyslipidemia and hypothyroidism in a population-based study. In this cross-sectional study, 2 315 dyslipidemic patients, aged 20-90 years (mean age: 38.1±13.2 years), were selected from among 5 760 participants of Tehran Thyroid Study and divided into 3 groups, the subclinical hypothyroid, overt hypothyroid, and euthyroid subjects, based on national reference ranges. Serum lipid profiles, free thyroxine (FT4), thyroid stimulating hormone (TSH), and thyroid peroxidase antibody (TPOAb) were measured in all subjects. In subjects with dyslipidemia and nondyslipidemia, the prevalence of subclinical was 7% and 4.1%, respectively, and for clinical hypothyroidism 3% and 1.2%, respectively. In dyslipidemic subjects, the mean low density lipoprotein-cholesterol (LDL-C) levels differed significantly (p=0.03) among the overt hypothyroid (144.3±36.1), subclinical hypothyroid (129.3±39.2), and euthyroid (132.7±39.0) groups. In the overt hypothyroid group, mean total cholesterol level was higher than in the normal group, but not significant. There were no differences in median triglycerides (TG) and mean high density lipoprotein-cholesterol (HDL-C) levels among the 3 groups mentioned. After adjusting for age and sex, hypothyroidism was not related to elevated serum lipid profiles in patient with dyslipidemia. In conclusion, there is significant difference in the prevalence of subclinical and clinical hypothyroidism between nondyslipidemic and dyslipidemic subjects; after adjustment for age and sex the presence of dyslipidemia did not predict the presence of hypothyroidism.
    Hormone and Metabolic Research 09/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Carvedilol is a novel β-adrenoreceptor blocker, with antioxidant properties inhibiting lipid peroxidation and preventing the depletion of endogenous antioxidants. Moreover, carvedilol was reported to enhance the expression of Bcl-2 gene, which has antioxidant and antiapoptotic effects. There are few researches testing the protective effect of carvedilol on the development of diabetic cardiomyopathy and nephropathy. In this study, we induced diabetes mellitus in male Wistar albino rats. We investigated carvedilol, as well as vitamin E, administrated in healthy and diabetic rats for 6 weeks to compare their effects on biochemical parameters and the expression of Bcl-2 protein in both myocardial and renal tissues by immunohistochemistry. The study showed that the diabetic rats not only had renal dysfunction and more myocardial damage, but also showed lower expression of Bcl-2 protein. Carvedilol and vitamin E treatments were associated with better renal function and less myocardial damage, lower blood glucose, and lipid peroxidation, higher antioxidant capacity, better serum lipids, and higher expression of Bcl-2 protein in diabetic rats. These results indicate that carvedilol and vitamin E treatments partly protect against myocardial and renal damage probably via their antioxidant and antiapoptotic properties in diabetic rats.
    Hormone and Metabolic Research 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Illegitimate G-protein coupled receptors are known to control cortisol secretion in adrenal adenomas and bilateral macronodular adrenal hyperplasias (BMAHs) causing Cushing's syndrome. In the present study, we have evaluated the role of glucagon in the regulation of cortisol secretion in 13 patients with BMAH or adrenocortical adenoma causing subclinical or overt Cushing's syndrome. Injection of glucagon provoked an increase in plasma cortisol in 2 patients. After surgery, immunohistochemical studies showed the presence of glucagon receptor-like immunoreactivity in clusters of spongiocytic cells in adrenal tissues from patients who were sensitive in vivo to glucagon. We also observed an in vitro cortisol response to vasoactive intestinal peptide from an adenoma, which was insensitive to glucagon and pituitary adenylate cyclase-activating peptide. Altogether, our data show that ectopic glucagon receptors are expressed in some adrenal cortisol-producing benign lesions. Our results also indicate that circulating glucagon may influence cortisol release under fasting conditions.
    Hormone and Metabolic Research 07/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hypogonadotropic hypogonadism (HH) is common in pituitary stalk interruption (PSI) patients. However, the optimal timing and effective regimen in the management of the pituitary-gonadal axis deficiency is still controversial. This study involved a retrospective review of 38 male patients with HH resulting from PSI. The HH patients were subdivided according to their ages into 2 experiment groups: Group I (adolescents, 14-18 years old, 25 cases) and Group II (young adults, 18-24 years old, 13 cases). To compare the therapeutic response to exogenous gonadotropin, a control analysis was carried out in the experimental groups with age-matched control groups. Before gonadotropin therapy, no significant increases in gonadal hormones were noted in either of the 2 experimental groups. After treatment with human chorionic gonadotropin (hCG) for less than 6 months, the hormone levels of pituitary-gonadal axis significantly increased in group I than in group II. After adding the human menopause gonadotropin (hMG) for 6 months, the gonadal hormone levels of group II were significantly increased. In addition, the Tanner stage and penis lengths in group I were significantly improved. There was no significant adverse impact on BMI and height velocity (HV) after less than one year therapy. A prolonged hypogonadotropic period without treatment may be responsible for testicular dysfunction in HH males caused by PSI. Early supplementary therapy with hCG and hMG is beneficial for the recovery of gonadal hormone and development of secondary sexual characteristics.
    Hormone and Metabolic Research 05/2014; 46(09).
  • [Show abstract] [Hide abstract]
    ABSTRACT: Major depressive disorder has been associated with low bone mineral density. The strength of this association, however, varies greatly among studies; the direction of the causative link is still controversial, and the etiology remains unclear. We aimed to confirm this association, assess its magnitude and estimate its clinical relevancy. A total of 535 articles were initially identified and the research synthesis was based on 33 qualified articles. Of these, 25 articles (or 76%) showed an inverse relationship between major depression or minor depression or depressive symptoms and bone mineral density or bone turnover. Meta-analysis could be performed on 20 of the initially selected 33 articles. Standardized weighted differences in mean AP spine, total femur and femoral neck bone mineral density, each from at least 10 studies, were computed in g/cm (2) and transformed into percent differences. At each site, bone mass was lower in subjects with depression as compared to controls: AP spine bone mineral density was 4.73% lower (95% CI -7.28% to -2.19%, p<0.0001; n=16 studies), total femur bone mineral density was 3.53% lower (95% CI -5.66% to -1.41%, p<0.001; n=13 studies), and femoral neck bone mineral density was 7.32% lower (95% CI -10.67% to -3.96%; p<0.0005; n=8 studies). In conclusion, major depressive disorder was associated with lower bone mineral density at the AP spine, femoral neck, and total femur. The deficits in bone mineral density in subjects with depression are of clinical significance and likely to increase fracture risk over the lifetime of these subjects.
    Hormone and Metabolic Research 06/2010; 42(7):467-82.
  • Hormone and Metabolic Research 01/2010; 42(12):822-886.