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Biochem J. 2002 Sep 15;366(Pt 3):757-66.
Hormone-specific regulation of the kidney androgen-regulated gene promoter in cultured mouse renal proximal-tubule cells.

Soler M, Tornavaca O, Sole E, Menoyo A, Hardy D, Catterall JF, Vandewalle A, Meseguer A.

Centre d'Investigacions en Bioquimica i Biologia Molecular (CIBBIM), Hospital Universitari Vall d'Hebron, 08035 Barcelona, Spain.

The kidney androgen-regulated protein (KAP) is specifically expressed and differentially regulated by androgens and tri-iodothyronine (T(3)) in intact mouse early (PCT) and late (PR) proximal-tubule cells. Until now, detailed characterization of the molecular elements mediating androgen-responsive gene expression in the kidney has been hampered by the lack of appropriate cultured cell systems suitable for DNA transfection studies. In the present study we have analysed the hormone-dependent transactivation of the KAP gene promoter in immortalized differentiated PCT and PR proximal-tubule cells derived from L-PK/Tag1 transgenic mice. Transient transfection studies with different KAP promoter constructs indicated that a 224 bp-truncated fragment was sufficient to mediate cell-specific expression of the KAP promoter. Dihydrotestosterone (DHT) stimulated in an androgen-dependent manner the transactivation of KAP in PCT and PR cells, while mutation of a putative androgen-response element (ARE) sequence located at -39 bp from the transcription initiation site abolished the transactivation induced by DHT. Furthermore, insulin-like growth factor 1 (IGF-1), but not T(3), enhanced the androgen-dependent transactivation of KAP in cultured PCT cells. These results demonstrate that the short 224 bp fragment of the KAP promoter is sufficient to drive the proximal-tubule androgen-specific regulated expression of KAP and reveal synergistic interactions between IGF-1 and androgens for KAP regulation in PCT cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12030848&dopt=Abstract

Clin Endocrinol (Oxf). 2002 May;56(5):603-7.
Use of GnRH agonist and human chorionic gonadotrophin tests for differentiating constitutional delayed puberty from gonadotrophin deficiency in boys.

Kauschansky A, Dickerman Z, Phillip M, Weintrob N, Strich D.

Institute of Endocrinology and Diabetes, Schneider Children's Medical Center of Israel, 14 Kaplan Street, Petah Tikva 49202, Israel.

OBJECTIVES: The differentiation of constitutional delayed puberty (CDP) from gonadotrophin deficiency (GD) in boys at referral poses a difficult challenge. The effectiveness of the GnRH agonist (GnRH-a) test in distinguishing between the two conditions was evaluated and compared with findings of the GnRH and hCG stimulation tests. PATIENTS, METHODS AND DESIGN: The study sample included 32 prepubertal boys aged 14 years or older. Thirteen entered spontaneous puberty within 1 year of referral (group A) and 19 remained prepubertal (group B). All underwent the GnRH test (Relefact, Hoechst AG, 0.1 mg/m2 i.v. in one bolus), GnRH-a test (Decapeptyl, Ferring GmbH, 0.1 mg/m2 s.c.) and hCG stimulation (Chorigon, Teva, 1500 units i.m. on three alternate days) at 1-week intervals. All tests were performed at referral at 0800 h. Blood samples were collected before testing and at 30 and 60 min (GnRH test) or 4 h (GnRH-a) for LH and FSH determination, and before testing and at 4 h (GnRH-a) or on the seventh day (hCG) after stimulation for serum testosterone measurement. RESULTS: The LH response to GnRH-a and the testosterone response to hCG stimulation were significantly higher in group A (LH, mean +/- SD 20.4 +/- 7.5 mIU/ml, range 10.8-32.6; testosterone, mean +/- SD 18.0 +/- 5.9 nmol/l, range 9.4-26, P < 0.0001) than in group B (LH, mean +/- SD 2.3 +/- 2.0 mIU/ml, range 0.7-6.9; testosterone, mean +/- SD 1.0 +/- 0.7 nmol/l, range 0.7-3.2), with no overlap between the groups. The cut-off for the LH response to GnRH-a was 8.0 mIU/ml, and for the testosterone response to hCG, 8 nmol/l. There were also significant differences between the groups in mean basal serum LH and FSH (LH, 1.1 +/- 0.5 vs. 0.6 +/- 0.2 mIU/ml, P < 0.05; FSH, 2.2 +/- 2.0 vs. 0.4 +/- 0.3 mIU/ml, P < 0.02) and their response to GnRH (LH, 11.4 +/- 4.4 vs. 2.7 +/- 1.1 mIU/ml, P < 0.0001; FSH, 5.1 +/- 3.4 vs. 2.5 +/- 2.4 mIU/ml, P < 0.0001), and mean serum testosterone level at 4 h after GnRH-a administration (1.9 +/- 1.0 vs. 0.9 +/- 0.4 nmol/l, P = 0.002), but all showed a great overlap in range. Mean age, testicular volume and basal serum testosterone levels were similar in the two groups at referral. One year later, the testicular volume of group A (5.0-12.0 ml) was significantly larger than that of group B (1.0-3.0 ml, P < 0.0001), which remained unchanged on re-examination 3.0 +/- 0.5 years later. CONCLUSIONS: The GnRH-agonist test and the repeated-injection hCG test are reliable diagnostic tools for differentiating CDP from GD in boys.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12030910&dopt=Abstract

Asian J Androl. 2002 Dec;4(4):295-8.
Effect of Withania somnifera root extract on the sexual behaviour of male rats.

Ilayperuma I, Ratnasooriya WD, Weerasooriya TR.

Department of Anatomy, Faculty of Medicine, University of Ruhuna, Sri Lanka.

AIM: To determine the effect of a methanolic extract of Withania somnifera (L.) Dunal roots on sexual competence of male rats. METHODS: Male rats were orally administered 3000 mg.kg-1.day-1 of root extract for 7 days. Their sexual behaviour was evaluated 7 days prior to treatment, day 3 and 7 of treatment, and day 7, 14 and 30 post-treatment by pairing each male with a receptive female. RESULTS: The root extract induced a marked impairment in libido, sexual performance, sexual vigour, and penile erectile dysfunction. These effects were partly reversible on cessation of treatment. These antimasculine effects are not due to changes in testosterone levels or toxicity but may be attributed to hyperprolactinemic, GABAergic, serotonergic or sedative activities of the extract. CONCLUSION: Use of W. somnifera roots may be detrimental to male sexual competence.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12508132&dopt=Abstract

Oral Microbiol Immunol. 2002 Jun;17(3):186-92.
Testosterone stimulates proliferation and inhibits interleukin-6 production of normal and hereditary gingival fibromatosis fibroblasts.

Coletta RD, Reynolds MA, Martelli-Junior H, Graner E, Almeida OP, Sauk JJ.

Department of Oral Pathology, University of Campinas Dental School, Caixa Postal 52, 13414-018 Piracicaba-SP, Sao Paulo, Brazil.

Hereditary gingival fibromatosis (HGF) is a rare oral condition characterized by a slow and progressive enlargement of the gingiva, involving both the maxilla and mandible. In vitro, HGF fibroblasts demonstrate a proliferative index significantly higher than fibroblasts from normal gingiva (NG). The objective of this study was to determine the effect of dihydrotestosterone on the proliferation of gingival fibroblasts derived from patients with HGF (n = 4) and from four healthy individuals. Additionally, we analyzed the effect of dihydrotestosterone on interleukin-6 (IL-6) production and determined the expression levels of androgen receptors in NG and HGF fibroblasts. Gingival fibroblasts from NG and HGF were incubated with increasing concentrations of dihydrotestosterone with or without androgen blockers, and cultured for 24 h, and the proliferation index was determined by automated cell counter. IL-6 production, in this system, was quantified using a "capture" enzyme-linked immunosorbent assay (ELISA). Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was performed to measure the mRNA expression of androgen receptors. The results indicated that dihydrotestosterone simultaneously downregulates the production of IL-6 and upregulates the cell proliferation. Finasteride and cyprosterone acetate, two anti-androgens, partially reversed these effects. Androgen receptor mRNA expression was identified in both NG and HGF fibroblasts; however, the levels in NG were higher than those observed in HGF. These results show that testosterone coordinates the proliferation and production of IL-6 of normal and HGF fibroblasts.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12030972&dopt=Abstract

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