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synthesis may take place not only in adrenals and ovaries but also in adipose tissue. Recent research focused on sex steroid conversion in human adipose tissue, specifically investigating the expression and activity of 17β
INSERM U716, Institut Universitaire d’Hématologie, Hôpital Saint-Louis/Bâtiment INSERM, 1 avenue Claude Vellefaux, 75010 Paris, France
Unité INSERM 540, Montpellier, France
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INSERM U716, Institut Universitaire d’Hématologie, Hôpital Saint-Louis/Bâtiment INSERM, 1 avenue Claude Vellefaux, 75010 Paris, France
Unité INSERM 540, Montpellier, France
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INSERM U716, Institut Universitaire d’Hématologie, Hôpital Saint-Louis/Bâtiment INSERM, 1 avenue Claude Vellefaux, 75010 Paris, France
Unité INSERM 540, Montpellier, France
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INSERM U716, Institut Universitaire d’Hématologie, Hôpital Saint-Louis/Bâtiment INSERM, 1 avenue Claude Vellefaux, 75010 Paris, France
Unité INSERM 540, Montpellier, France
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INSERM U716, Institut Universitaire d’Hématologie, Hôpital Saint-Louis/Bâtiment INSERM, 1 avenue Claude Vellefaux, 75010 Paris, France
Unité INSERM 540, Montpellier, France
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INSERM U716, Institut Universitaire d’Hématologie, Hôpital Saint-Louis/Bâtiment INSERM, 1 avenue Claude Vellefaux, 75010 Paris, France
Unité INSERM 540, Montpellier, France
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INSERM U716, Institut Universitaire d’Hématologie, Hôpital Saint-Louis/Bâtiment INSERM, 1 avenue Claude Vellefaux, 75010 Paris, France
Unité INSERM 540, Montpellier, France
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cells but activated an estrogen response element luciferase construct (data not shown). Thus, E 2 does not directly modulate Flk-1/KDR in endothelial cells; a direct effect of E 2 could be limited to the vasculature of sex steroid-responsive tissues
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serum E 2 in the artery is then elevated by BDL. Some liver microsomal CYPs are maintained by serum sex steroid hormones ( Dueland et al . 1991 , Chen et al . 1995 , Chico et al . 1996 ). Male-specific CYP genes, Cyp2c55 and C yp 3a2 , are down
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profoundly during the third trimester when the plasma estrogen level is highest ( Whitacre 2001 ). Therefore, the sex steroid hormones, primarily estrogens, have been suggested to be responsible for the sex difference in prevalence and presentation of
Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición S. Zubirán, México City, México
Department of Reproductive Biology, Universidad Autónoma Metropolitana Iztapalapa, Av. San Rafael Atlixco 186, Colonia Vicentina, Delegación Iztapalapa, México City, México
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Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición S. Zubirán, México City, México
Department of Reproductive Biology, Universidad Autónoma Metropolitana Iztapalapa, Av. San Rafael Atlixco 186, Colonia Vicentina, Delegación Iztapalapa, México City, México
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Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición S. Zubirán, México City, México
Department of Reproductive Biology, Universidad Autónoma Metropolitana Iztapalapa, Av. San Rafael Atlixco 186, Colonia Vicentina, Delegación Iztapalapa, México City, México
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Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición S. Zubirán, México City, México
Department of Reproductive Biology, Universidad Autónoma Metropolitana Iztapalapa, Av. San Rafael Atlixco 186, Colonia Vicentina, Delegación Iztapalapa, México City, México
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Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición S. Zubirán, México City, México
Department of Reproductive Biology, Universidad Autónoma Metropolitana Iztapalapa, Av. San Rafael Atlixco 186, Colonia Vicentina, Delegación Iztapalapa, México City, México
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Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición S. Zubirán, México City, México
Department of Reproductive Biology, Universidad Autónoma Metropolitana Iztapalapa, Av. San Rafael Atlixco 186, Colonia Vicentina, Delegación Iztapalapa, México City, México
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Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición S. Zubirán, México City, México
Department of Reproductive Biology, Universidad Autónoma Metropolitana Iztapalapa, Av. San Rafael Atlixco 186, Colonia Vicentina, Delegación Iztapalapa, México City, México
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Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición S. Zubirán, México City, México
Department of Reproductive Biology, Universidad Autónoma Metropolitana Iztapalapa, Av. San Rafael Atlixco 186, Colonia Vicentina, Delegación Iztapalapa, México City, México
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, Musgrove & Sutherland 1994 , Pasqualini & Chetrite 1996 , Girdler & Brotherick 2000 ); however, the precise involvement of other sex steroid hormones on this malignancy has remained a controversial issue. Evidence has accumulated indicating that androgens
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GnRH and sex steroids play an important role in immune system modulation and development. GnRH and the GnRH receptor are produced locally by immune cells, suggesting an autocrine role for GnRH. Experimental studies show a stimulatory action of exogenous GnRH on the immune response. The immune actions of GnRH in vivo are, however, less well established. Oestrogen and androgen receptors are expressed in primary lymphoid organs and peripheral immune cells. Experimental data have established that oestrogens enhance the humoral immune response and may have an activating role in autoimmune disorders. Testosterone enhances suppressor T cell activity. Although there are some clinical studies consistent with these findings, the impact of sex steroids in autoimmune disease pathogenesis and the risk or benefits of their usage in normal and autoimmune-disordered patients remain to be elucidated. There are neither experimental nor clinical data evaluating functional GnRH-sex steroid interactions within the human immune system, and there is a paucity of data relating to GnRH analogues, hormone replacement therapy and oral contraceptive and androgen action in autoimmune diseases. However, a growing body of experimental evidence suggests that an extra-pituitary GnRH immune mechanism plays a role in the programming of the immune system. The implications of these findings in understanding immune function are discussed.
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Abstract
In many mammalian species, circulating levels of insulinlike growth factor-I (IGF-I) rise during puberty. Previous studies manipulating testosterone levels in rats with normal GH secretion suggested that the pubertal IGF-I rise is regulated by an interaction between GH and sex steroids. Therefore, in a reciprocal study, IGF-I levels were examined during sexual maturation of the GH-deficient dwarf (dw/dw) rat which has a selective genetic deficiency of GH but normal sex steroid levels. Male dw/dw rats were treated with daily injections of recombinant human GH (200 μg/100 g body weight) or saline vehicle, from 28 to 70 days of age. Sexual maturation was determined to occur primarily between 42 and 63 days of age based on testis and seminal vesicle growth and plasma testosterone levels. GH treatment had no effect on seminal vesicle weights, plasma testosterone or gonadotrophins. GH administration resulted in a 7% increase in absolute testes weight (P<0·05), but a 50% increase in body weight (P<0·0001). These results supported previous findings that the reproductive development of dw/dw rats is essentially normal. Untreated dw/dw rats had no rise in IGF-I levels during sexual maturation. In contrast, treatment with GH produced a marked sustained rise in IGF-I levels (P<0·0001). Ligand blots demonstrated GH induction of IGF-binding protein-3 (IGFBP-3) and an IGFBP cluster at 32 kDa. The initially high immunoreactive IGFBP-1 levels (>600 ng/ml) decreased by 49 days of age after which untreated dw/dw rats had significantly higher IGFBP-1 levels than GH-treated dw/dw rats (P<0·01). We conclude that GH secretion, rather than sex steroids, may be the predominant determinant of pubertal IGF-I levels in rats and that the rise in circulating IGF-I levels during puberty is not an indispensible event for normal reproductive development.
Journal of Endocrinology (1994) 141, 393–401
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SUMMARY
Basal gonadotrophin and sex steroid levels and responses to an intravenous injection of 100 μg gonadotrophin releasing hormone (Gn-RH) have been studied in 15 patients with polycystic ovaries. Mean basal LH concentration was raised and an excessive, exaggerated and prolonged response was observed after Gn-RH treatment, but patients could further be subdivided into two functional groups on the basis of their basal LH values and LH response patterns. Evidence was also produced which suggested a breakdown in the negative feedback mechanism in these patients.
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Sex steroids are required for a normal pubertal growth spurt and fusion of the human epiphyseal growth plate. However, the localization of sex steroid receptors in the human pubertal growth plate remains controversial. We have investigated the expression of estrogen receptor (ER) alpha, ERbeta and androgen receptor (AR) in biopsies of proximal tibial growth plates obtained during epiphyseal surgery in 16 boys and eight girls. All pubertal stages were represented (Tanner stages 1-5). ERalpha, ERbeta and AR were visualized with immunohistochemistry and the number of receptor-positive cells was counted using an image analysis system. Percent receptor-positive chondrocytes were assessed in the resting, proliferative and hypertrophic zones and evaluated for sex differences and pubertal trends. Both ERalpha- and ERbeta-positive cells were detected at a greater frequency in the resting and proliferative zones than in the hypertrophic zone (64+/-2%, 64+/-2% compared with 38+/-3% for ERalpha, and 63+/-3%, 66+/-3% compared with 53+/-3% for ERbeta), whereas AR was more abundant in the resting (65+/-3%) and hypertrophic zones (58+/-3%) than in the proliferative zone (41+/-3%). No sex difference in the patterns of expression was detected. For ERalpha and AR, the percentage of receptor-positive cells was similar at all Tanner pubertal stages, whereas ERbeta showed a slight decrease in the proliferative zone during pubertal development (P<0.05). In summary, our findings suggest that ERalpha, ERbeta and AR are expressed in the human growth plate throughout pubertal development, with no difference between the sexes.
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Sex steroid hormones exert important biological effects on the brain. Moreover, an extensive sex steroid metabolism occurs in the brain. In sex steroid metabolism 17beta-hydroxysteroid dehydrogenases (17beta-HSDs) play essential roles in catalyzing the final steps in androgen and estrogen biosynthesis. Recently four types of human 17beta-HSDs and a pseudogene of the type 1 isoform were identified. To date, 17beta-HSD has not been extensively studied in the human brain. Therefore, we investigated the mRNA expression of the four isozymes of 17beta-HSD as well as the pseudogene of the type 1 isoform in the human temporal lobe to determine the predominant isoforms and, moreover, to elucidate the existence of possible sex and age differences. We studied biopsy materials from the temporal lobe of 34 women, 32 men and 10 children. Quantification of different mRNAs was achieved by competitive reverse transcription-PCR. 17beta-HSD 1, 17beta-HSD 3 and 17beta-HSD 4 were expressed in the human temporal lobe of children and adults, whereas 17beta-HSD 2 and the pseudogene of 17beta-HSD 1 were not expressed. In adults, 17beta-HSD 3 and 17beta-HSD 4 mRNA concentrations were significantly higher in the subcortical white matter (17beta-HSD 3: 14 591+/-3457 arbitrary units (aU), mean+/-s.e.m.; 17beta-HSD 4: 1201+/-212 aU) than in the cortex (17beta-HSD 3: 5428+/-1057 aU, P<0. 0002; 17beta-HSD 4: 675+/-74 aU, P<0.004). 17beta-HSD 1 concentrations did not differ significantly between the white matter (3860+/-1628 aU) and the cortex (2525+/-398 aU) of adults. In conclusion, the present study demonstrates the expression of 17beta-HSD 1, 3 and 4 mRNAs in the human temporal lobe. Together with CYP19AROM and 5alpha-reductase, known to be expressed in the human brain, the expression of 17beta-HSD 1, 3 and 4 mRNAs indicates the major importance of local steroid biosynthesis in the brain.
