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Interferon research abs 1 || Hemoglobin research abs || Stem cell research abs || Nucleic acid research abs || Herpes research abs || Bronchitis research abs || Schizophrenia research abs || Tuberculosis research abs || Pneumonia research abs || Constipation research abs || Laxative research abs || hair research abs || hair related research references || testosterone related research references

Clin Nephrol. 2002 Dec;58(6):431-7.
Relationship between body composition, sex hormones and leptinemia in hemodialyzed patients with chronic renal failure.

Chudek J, Adamczak M, Kokot F, Karkoszka H, Ignacy W, Klimek D, Wiecek A.

Department of Nephrology, Endocrinology and Metabolic Diseases, Silesian University Medical School, Katowice, Poland.

BACKGROUND: Females are characterized by significantly higher plasma leptin concentration than males. It seems likely that sex hormones influence leptinemia independently from differences in body composition. The aim of the present study was to analyze the contribution of plasma concentrations of testosterone and estradiol on leptinemia in hemodialyzed patients. METHODS: 110 hemodialyzed patients--HD (60 M, 50 F) and 70 healthy subjects (HS) (30 M, 40 F) were enrolled in this study. Plasma leptin, testosterone or estradiol and CRP concentrations and body composition by dual-energy X-ray absorptiometry (DEXA) were assessed. RESULTS: Total body fat was significantly higher in females than in males (27.5 +/- 1.5% vs. 17.2 +/- 1.0% of body weight in HD and 36.0 +/- 1.0% vs. 18.2 +/- 1.4% in HS, respectively). Plasma leptin concentrations were markedly higher in females than in males both in HD (27.9 +/- 5.4 ng/ml vs. 9.6 +/- 1.9 ng/ml) and HS (16.5 +/- 1.7 ng/ml vs.3.1 +/- 0.4 ng/ml). A highly significant, strong positive correlation was found between total fat mass (TFM) and leptinemia in all studied groups. No significant univaried correlation between plasma leptin and testosterone or estradiol concentrations respectively was found both in HD and HS. Multiple regression analyses showed that the main determinant of leptinemia is TFM (beta = 0.623 and 0.798 in HS females and males respectively, and beta = 1.058 and 0.797 in HD females and males respectively). Plasma concentration of testosterone (beta = -0.139 and beta = -0.075 in male HD and HS respectively) and estradiol (beta = 0.199 and beta = 0.046 in females HD and HS, respectively) contributed to leptinemia only in a minor degree. CONCLUSION: Both testosterone and estradiol are minor contributors to leptinemia both in HS and HD patients. The main determinant of leptinemia in these subjects is total body fat mass.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12508965&dopt=Abstract

Diabetes Obes Metab. 2002 May;4(3):209-13.
The regulation of HSL and LPL expression by DHT and flutamide in human subcutaneous adipose tissue.

Anderson LA, McTernan PG, Harte AL, Barnett AH, Kumar S.

Department of Medicine, University of Birmingham, Division of Medical Sciences, Edgbaston, Birmingham, UK.

Clinical observations suggest a role for testosterone in the accumulation of central adiposity and with an associated increased risk of disease. To date, no human study has analysed the role of dihydrotestosterone (DHT) on adipose tissue mass regulation in vitro. This study investigated the role of DHT and androgen receptors (AR) in the regulation of lipolysis and lipogenesis by examining the key enzymes hormone sensitive lipase (HSL) and lipoprotein lipase (LPL) respectively. Isolated abdominal subcutaneous adipocytes (Scad) (n = 15) were treated with either DHT (10(-7)-10(-9) m), an antiandrogen, flutamide (FLT: 10(-7)-10(-9) m) or a combination of DHT (10(-7)-10(-9) m) with FLT (10(-8) m). Relative protein expression of HSL, LPL and AR was determined. In Scad, DHT inhibited HSL expression maximally at 10(-9) m (0.7 +/- 0.4**; p < 0.01**) compared with control (control: 1.0 +/- (s.e.m.) 0.0), whereas LPL protein expression was stimulated at DHT10(-9) m (2.22 +/- 0.48*; p < 0.05*). Glycerol release assay results correlated with HSL expression data. LPL expression was reduced at all doses with combinations of DHT + FLT compared with DHT alone. Androgen receptor expression studies showed an inverse correlation with DHT, whereas DHT + FLT reduced AR expression. These studies indicate that DHT may alter HSL and LPL expression, whereas only LPL expression appears mediated by AR. These findings suggest a physiological role for DHT in the control of adipose tissue mass in women, and indicate that androgens may also play an important role in regulating lipid metabolism.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12047400&dopt=Abstract

Anim Reprod Sci. 2002 Jun 17;71(3-4):203-15.
Passive immunization of rams (Ovis aries) against GnRH: effects on antibody titer, serum concentrations of testosterone, and sexual behavior.

Parthasarathy V, Price EO, Orihuela A, Dally MR, Adams TE.

Department of Animal Science, University of California, Davis, CA 95616, USA. vallrches.uga.edu

The effect of immunoneutralization of gonadotropin-releasing hormone (GnRH) on serum concentrations of testosterone and sexual behavior was evaluated in sexually mature male sheep. In Experiment 1, GnRH1 rams (n=16) were passively immunized against GnRH (300 ml antiserum), control rams were either passively immunized against keyhole limpet hemocyanin (KLH, n=15) or surgically castrated (Wethers1, n=4). Sexual performance of the rams was assessed weekly for 3 weeks before and 6 weeks after immunization, using ovarihystertomized ewes actively immunized against GnRH. Experiment 2 evaluated the effects of repeated immunization. Rams were immunized with two aliquots (400 and 300 ml, respectively) of anti-GnRH sera (GnRH, n=5) or normal sheep serum (NSS, n=4), 2 weeks apart. Surgically castrated animals were used as a second control group (Wethers2). Administration of anti-GnRH sera, but neither anti-KLH nor NSS sera, resulted in marked reduction (P<0.05) in serum concentrations of testosterone. Sexual behavior was not consistently affected by administration of one aliquot of anti-GnRH sera, however repeated immunizations resulted in more persistent reduction in serum concentrations of testosterone and more consistent suppression of sexual behavior.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12047929&dopt=Abstract

J Biol Chem. 2002 Aug 16;277(33):29600-7. Epub 2002 Jun 04.
Nongenomic testosterone calcium signaling. Genotropic actions in androgen receptor-free macrophages.

Guo Z, Benten WP, Krucken J, Wunderlich F.

Division of Molecular Parasitology and the Centre of Biological Medical Research, Heinrich-Heine University, 40225, Dusseldorf, Germany.

Steroid hormones exert genotropic actions through members of the nuclear receptor family. Here, we have demonstrated genotropic actions of testosterone that are independent of intracellular androgen receptors (iAR). Through plasma membrane androgen receptors (mAR), testosterone induces a rapid rise in the intracellular free Ca(2+) concentration of iAR-free murine RAW 264.7 macrophages. This nongenomic testosterone signaling, which is independent of both iAR and estrogen receptors, does not in itself activate either the mitogen-activated protein kinase (MAPK) families ERK1/2, p38, and JNK/SAPK, the stably and transiently transfected c-fos promoter, or NO production. In the context of lipopolysaccharide (LPS) signaling, however, testosterone attenuates LPS activation of the c-fos promoter and NO production, which is abolished by the intracellular Ca(2+) chelator BAPTA. Testosterone also attenuates the LPS activation of p38 but not that of ERK1/2 and JNK/SAPK, and this attenuation is abrogated by BAPTA. Moreover, the p38 inhibitor, SB 203580, largely reduces LPS activation of the c-fos promoter and NO production, and the remaining levels are no longer regulated by testosterone. This study is the first to provide information on genotropic actions of mAR-mediated nongenomic testosterone Ca(2+) signaling by cross-talk with the LPS signaling pathway through p38 MAPK with impact on cell function.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12048191&dopt=Abstract

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