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. 1978 , Maclaren et al. 1980 , Kava et al. 1992 , Shi et al. 1994 , Weksler-Zangen et al. 2001 ). Removal of testosterone from the sex-steroid milieu of the male animal improved insulin sensitivity in most studies, and thus was protective
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Centro de Biología Molecular ‘Severo Ochoa’, Departamento de Neuropatología Molecular CSIC-UAM, Madrid, Spain
Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain
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Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain
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activates c-Src family tyrosine kinases . Molecular Cell 8 269 – 280 . ( https://doi.org/10.1016/S1097-2765(01)00304-5 ) 10.1016/S1097-2765(01)00304-5 11545730 Bourque M Dluzen DE Di Paolo T 2009 Neuroprotective actions of sex steroids in
Department of Medicine, Christchurch School of Medicine and Health Sciences, University of Otago, Christchurch, New Zealand
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Department of Medicine, Christchurch School of Medicine and Health Sciences, University of Otago, Christchurch, New Zealand
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Department of Medicine, Christchurch School of Medicine and Health Sciences, University of Otago, Christchurch, New Zealand
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Department of Medicine, Christchurch School of Medicine and Health Sciences, University of Otago, Christchurch, New Zealand
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Department of Medicine, Christchurch School of Medicine and Health Sciences, University of Otago, Christchurch, New Zealand
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peptide and the sex steroid increased the number of cells that secreted adrenomedullin, both hormones induced an increase in the mean level of expression of adrenomedullin mRNA (Fig. 5 ), the effect being statistically significant for testosterone
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Introduction Sex steroids are mainly synthesized by the gonads (testis and ovary), but the adrenals constitute an additional source ( Vanderschueren et al . 2004 , Callewaert et al . 2010 a ). Sex steroids are involved in the regulation of a
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Department of Physiology, Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Kiinamyllynkatu 10, FI-20014 Turku, Finland
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Department of Physiology, Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Kiinamyllynkatu 10, FI-20014 Turku, Finland
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Department of Physiology, Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Kiinamyllynkatu 10, FI-20014 Turku, Finland
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Introduction Imbalanced action of sex steroid hormones, i.e. androgens and estrogens, is involved in the pathogenesis of various severe diseases in humans. Hormone-dependent cancers are commonly lethal both in women and in men, with breast cancer
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important to understand the physiological function of this highly restricted tissue-specific gene to gain insight into the physiological effects of sexual steroids in the kidney. In this report, we further explored the tissue distribution and sex-steroid
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enzymes whose activity is influenced by sex steroids ( Spike et al. 1992 , Gibson et al. 1999 , Coto-Montes et al. 2001 ). In fact, the female hamster has considerably more porphyrins than the male ( Spike et al. 1985 , 1986 ). These
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clarified. It is well known that a variety of circulating hormones have the potential to affect linear growth and bone formation ( van der Eerden et al . 2003 ). For example, in humans sex steroids have important actions during puberty to enhance linear
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estriol. E 2 is the most active estrogen and the predominant female sex steroid during the reproductive years. In addition to these classical estrogens, there are various other steroidal and non-steroidal compounds that are able to interact with estrogen
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Histamine is synthesized in cells by histidine decarboxylase (HDC). HDC-deficient knockout (KO) mice lack functional HDC and histamine in the tissues. In the present study we used this in vivo model for studying the role of HDC deficiency in the regulation of male steroid hormone metabolism. In agreement with earlier studies showing the lack of effects of central histamine on the basal secretion of gonadotrope hormones, we found no difference with in situ hybridization in the expression of GnRH in the hypothalamus of wild type and KO mice. The tissue concentrations of testosterone and several androgenic steroids were significantly elevated in the testes but not in the adrenal glands of HDC-KO mice. In contrast, serum estradiol levels failed to show a significant difference between the two groups. The weight of the testes was significantly smaller in both 7-day-old and adult KO mice. The ultrastructure of the adult testis indicated elevated steroid synthesis with more tightly coiled membranous whorls in Leydig cells. The present results suggest that changes in reproductive functions and sex steroid secretion in male HDC-KO mice are not due to altered hypothalamic GnRH expression but are probably related to definite modifications during fetal development of KO mice reinforced later by the lack of the effect of peripheral histamine. This may provide in vivo evidence that peripheral histamine is an important regulatory factor of male gonadal development during embryogenesis and of sex steroid metabolism later in adulthood.
