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      Identification of Sex Hormone-Binding Globulin in the Human Hypothalamus

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          Gonadal steroids are known to influence hypothalamic functions through both genomic and non-genomic pathways. Sex hormone-binding globulin (SHBG) may act by a non-genomic mechanism independent of classical steroid receptors. Here we describe the immunocytochemical mapping of SHBG-containing neurons and nerve fibers in the human hypothalamus and infundibulum. Mass spectrometry and Western blot analysis were also used to characterize the biochemical characteristics of SHBG in the hypothalamus and cerebrospinal fluid (CSF) of humans. SHBG-immunoreactive neurons were observed in the supraoptic nucleus, the suprachiasmatic nucleus, the bed nucleus of the stria terminalis, paraventricular nucleus, arcuate nucleus, the perifornical region and the medial preoptic area in human brains. There were SHBG-immunoreactive axons in the median eminence and the infundibulum. A partial colocalization with oxytocin could be observed in the posterior pituitary lobe in consecutive semithin sections. We also found strong immunoreactivity for SHBG in epithelial cells of the choroid plexus and in a portion of the ependymal cells lining the third ventricle. Mass spectrometry showed that affinity-purified SHBG from the hypothalamus and choroid plexus is structurally similar to the SHBG identified in the CSF. The multiple localizations of SHBG suggest neurohypophyseal and neuroendocrine functions. The biochemical data suggest that CSF SHBG is of brain rather than blood origin.

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          Most cited references 21

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          Transport of protein-bound hormones into tissues in vivo.

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            Elevated sex-hormone binding globulin in elderly women with Alzheimer's disease.

            Hormone levels change significantly with increasing age. These changes may be related to, or be associated with, the emergence of age-related diseases, such as Alzheimer's disease (AD). Five hundred and seventy-six women over the age of 65 were studied from the Washington Heights-Inwood Columbia Aging Project (WHICAP). These women were selected from a group of healthy Medicare beneficiaries that were aged 65 and older living in the geographically defined area of northern Manhattan in New York City. Serum levels of estrone (E1), estradiol (E2), total testosterone (TT), dehydroepiandosterone (DHEA), luteinizing hormone (LH), follicle stimulating hormone (FSH), and sex-hormone binding globulin (SHBG) were measured. Significant differences were found between patients with AD and controls only in the level of SHBG, which was 20% higher in patients compared to controls (68.5nmol/l versus 54.7nmol/l, P<0.001). We also estimated levels of total E2 because after menopause, E2 is largely derived from E1. AD patients had significantly lower levels of estimated E2 (AD 0.46 versus controls 0.49, P<0.01). Differences remained significant after adjusting for age, ethnic group, education, and body mass index (BMI). A marked increase in SHBG levels was found in AD patients. SHBG normally responds to circulating testosterone and estrogen, therefore, elevated SHBG suggests an abnormal increase in its production and regulation. Further work is needed to clarify the cause and consequences of this observation.
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              Testosterone-estradiol-binding globulin binds to human prostatic cell membranes


                Author and article information

                S. Karger AG
                October 2005
                02 November 2005
                : 81
                : 5
                : 287-293
                aLudwig-Maximilian-Universität München, Department of Biology 2, Munich, Germany; bFriedrich-Schiller-Universität Jena, Department of Anatomy 2, Jena, Germany; cUniversity of Illinois at Rockford, Department of Biomedical Science, Rockford, Ill., USA; dFriedrich-Schiller Universität-Jena, CUCA, Department of Human Genetics and Anthropology, Jena, Germany, eOtto-von-Guericke-Universität Magdeburg, Department of Psychiatry, Magdeburg, Germany, and fClinical Biochemistry Unit, Canterbury Health Laboratories, Christchurch, New Zealand
                88170 Neuroendocrinology 2005;81:287–293
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 5, References: 31, Pages: 7
                Original Paper


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