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S R Plymate

Publications and source records attributed to S R Plymate.

At least 37 records · Page 2Linked to original sources
PubMed1996

Insulin-like growth factor-binding protein-2 and -3 expression in benign human prostate epithelium, prostate intraepithelial neoplasia, and adenocarcinoma of the prostate.

Insulin-like growth factor (IGF)-binding proteins (IGFBPs) modulate the activity of IGFs. In vitro human prostate epithelial cells secrete IGFBP-2 and -3. In vivo IGFBP-2 is increased, and IGFBP-3 is decreased in the serum of patients with prostate cancer. Immunohistochemistry and in situ hybridization were performed to compare the expression of IGFBP-2 and -3 in vivo in prostate tissue containing benign epithelium, high grade prostate intraepithelial neoplasia (PIN), and adenocarcinoma. Immunoreactivity and messenger ribonucleic acid (mRNA) hybridization signals for IGFBP-2 and -3 were localized to epithelial cells. IGFBP-2 immunostaining intensity was significantly increased in PIN regions compared to that in normal epithelium and was further increased in malignant cells. IGFBP-2 mRNA was also significantly increased in PIN and cancer cells. IGFBP-3 immunoreactivity was significantly increased in PIN regions compared to normal epithelium; however, IGFBP-3 protein was significantly decreased in malignant cells. IGFBP-3 mRNA remained virtually unchanged in benign epithelium, PIN, and adenocarcinoma cells. These results demonstrate that increased IGFBP-2 protein in PIN and malignant cells is probably due to increased mRNA expression. However, levels of IGFBP-3 protein may be due to pre- and/or posttranslational mechanisms, including proteolysis. The changes in IGFBP-2 and -3 protein levels in prostatic tissue are in agreement with serum changes reported in patients with prostate cancer.

Adenocarcinoma↗
PubMed1996

The effect on the insulin-like growth factor system in human prostate epithelial cells of immortalization and transformation by simian virus-40 T antigen.

The insulin-like growth factor (IGF) system has been demonstrated to be important for proliferation and differentiation in tissues. This system has also been demonstrated to be an important regulator of the growth of normal prostate epithelium and has been implicated in the process of transformation to human epithelial prostate cancer. This study examined the function of the various components of the IGF system in benign prostate epithelium (BPE), simian virus-40 (SV40)-T antigen-immortalized prostate epithelial cells, P69SV40-T (P69), and two sublines generated from the parental line by serial passage through athymic mice: one tumorigenic (M2182) and one metastatic (M12). IGF-II messenger ribonucleic acid (mRNA) and protein were detected in BPE cells, and each of the three P69 cell lines. IGF-II protein levels were significantly higher in medium collected from the P69, M2182, and M12 cells than in BPE. Proliferation in response to IGF was P69 > BPE > M2182 > M12. The proliferative responses in the four cell types were paralleled by an increase in c-jun. In addition, as the cells became progressively more tumorigenic, the basal level of c-jun mRNA increased. IGF-binding protein-2 (IGFBP-2), -3, -4, -5, and -6 could be detected in the primary epithelial cell medium; however, as the cells became progressively more tumorigenic, there was a decrease in IGFBP-2, -3, -5, and -6 in the medium. The type 1 IGF receptor (IGFr) also decreased as the cells became more tumorigenic. The M12 cells had 80% fewer receptors than the P69 cells and 70% fewer than M2182 cells. There was no change in the Kd for IGF between the cell lines. Based on these data it would appear that the difference in proliferation between the BPE cells and P69s may be due to an increased concentration of inhibitory IGFBPs in the P69 medium. The decrease in proliferation seen in response to IGF in M2182 and M12 cells compared to the P69s would appear at least in part to be due to a decreased IGFr number. IGFr mRNA is represented by 11.0- and 7.0-kilobase bands in the BPE and P69 cells, but only by an 11.0-kilobase band in M2182 and M12 cells. These data indicate that there are significant changes that occur in the IGF system during the process of malignant transformation of the prostate epithelium. The changes described in the P69 cell system are similar to those seen in vivo and suggest that an intact IGF system may be important in maintaining a differentiated epithelial cell.

Animals↗
PubMed1996

Protein and messenger ribonucleic acid (mRNA) for the type 1 insulin-like growth factor (IGF) receptor is decreased and IGF-II mRNA is increased in human prostate carcinoma compared to benign prostate epithelium.

Insulin-like growth factors (IGFs) and the type 1 IGF receptor (IGF-R) are involved in normal growth and development of the human prostate. Changes in levels of IGF-R and IGFs have been shown for several malignancies. Immunohistochemistry and in situ hybridization were performed to compare the expression of IGF-R and IGF-II in vivo in prostate tissue containing benign epithelium, high grade prostate intraepithelial neoplasia (PIN), and adenocarcinoma. Messenger ribonucleic acid (mRNA) hybridization signals and immunoreactivity for IGF-R were localized primarily to epithelial cells, with less signal in stroma. IGF-R mRNA was significantly decreased by 42% in PIN and 35% in cancer cells compared to that in benign epithelium (P < 0.0001). IGF-R immunostaining was significantly decreased by 32% in PIN and by 42% in malignant epithelium compared to that in benign epithelium (P < 0.004). IGF-II mRNA was also localized primarily to epithelial cells. IGF-II mRNA was significantly increased by 30% in adenocarcinoma compared to that in benign epithelium (P < 0.03). Immunoreactivity for IGF-II was localized to both stroma and epithelium. Protein levels for IGF-II were not significantly increased in cancer cells compared to those in benign epithelium. The decrease in the type 1 IGF receptor and increase in IGF-II mRNA may affect prostate cancer proliferation and differentiation.

Adenocarcinoma↗
PubMed1996

Insulin-like growth factor-binding proteins (IGFBP)-4, -5, and -6 in the benign and malignant human prostate: IGFBP-5 messenger ribonucleic acid localization differs from IGFBP-5 protein localization.

Insulin-like growth factor (IGF)-binding proteins (IGFBPs) modulate the actions of IGF. We have previously reported that IGFBP-2 messenger ribonucleic acid (mRNA) and protein are increased, and IGFBP-3 protein decreased in malignant prostate epithelium compared to benign epithelium. In this study, we examined the other IGFBPs secreted by prostate cells in vitro, namely IGFBP-4, -5, and 6. Immunoreactivity and mRNA signals for IGFBP-4 and -6 were localized to epithelial cells, with less signal in stroma. IGFBP-4 immunostaining and hybridization signal were significantly increased in prostate adenocarcinoma compared to those in benign epithelium. Immunostaining for IGFBP-5 was localized to the epithelium and stroma. IGFBP-5 immunoreactivity was significantly increased in malignant compared to benign epithelium. IGFBP-5 mRNA signal was not localized to epithelial cells; rather, the signal was over stromal cells surrounding the acinar structures. These cells are thought to be fibroblasts. We show that IGFBP-4 mRNA and protein and IGFBP-5 protein are increased in malignant epithelium compared to benign epithelium, that IGFBP-6 is present in benign and malignant epithelium, and that there is differential localization of IGFBP-5 mRNA and protein in prostate tissue. IGFBP-5 that is made by fibroblasts appears to be sequestered by epithelial cells. IGFBP-5 may, therefore, be a factor in cellular interactions between stromal and epithelial cells that are of fundamental importance for normal prostatic development and function.

Aged↗
PubMed1996

Proteolysis of insulin-like growth factor-binding protein-3 in the male reproductive tract.

Insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) is produced by prostate epithelial and stromal cells and either enhances or inhibits the effects of IGF on prostate epithelial cells. The levels of this protein in the male reproductive tract may be determined in part by proteases, including prostate-specific antigen (PSA), produced by the prostate epithelium. In this study we examined the proteolytic activity of human seminal fluid on IGFBP-3. Seminal fluid and prostate massage fluid (PF) were examined for IGFBP-3 or its fragments by use of an IGFBP-3 RIA that detects intact IGFBP-3 as well as fragments, a two-site immunoradiometric assay (IRMA) that detects intact IGFBP-3 and the larger fragments, Western ligand blots (WLB), and immunoblots (WIB). In seminal fluid, IGFBP-3 was readily detectable by RIA, but was detected in only 50% of the samples assayed by IRMA. No detectable IGFBP-3 was observed by WLB with [125I]IGF-I as the ligand, but with IGF-II as the ligand, IGFBP-3 fragments at 16-17 kDa were noted. On WIB, the 16-kDa fragment of IGFBP-3 was most abundant, with a smaller amount of the 29-kDa fragment, but no intact IGFBP-3. These results indicated that most of the IGFBP-3 detected in seminal fluid was in small (< or = 16-kDa) fragments. When three or more seminal fluid samples collected 1 month apart were available from the same individual, the coefficient of variation was 10.0 +/- 1.26% (+/- SE) for IGFBP-3 by RIA vs. 73.3 +/- 11.2% for sperm counts in the same samples. In a group of 42 PF samples, the IGFBP-3 levels measured by either RIA or IRMA were approximately 3-fold higher than those in seminal fluid. Intact IGFBP-3 was detected by both WLB and WIB. There was a significant inverse correlation between PSA and IGFBP-3, measured by IRMA, in PF (r = -0.526; P < or = 0.004). Finally, in the PF of African-American men, PSA was significantly lower, and IGFBP-3 determined by IRMA was significantly higher compared to those in Caucasian men.

Blotting, Western↗
PubMed1996

Nandrolone, a 19-nortestosterone, enhances insulin-independent glucose uptake in normal men.

The effect of exogenous androgens on glucose metabolism is controversial. This study was designed to clarify the impact of testosterone enanthate (TE), an aromatizable androgen, and nandrolone decanoate (ND), a nonaromatizable androgen, on glucose disposal. Eleven healthy men were enrolled in a randomized, double-blind cross-over study. All subjects completed two treatment cycles consisting of two weekly injections of placebo followed by six weekly injections of either TE (300 mg/week) or ND (300 mg/week). Treatment periods were separated by a 4-week washout. A tolbutamide-modified, frequently sampled, iv glucose tolerance test was used to assess insulin-dependent and insulin-independent glucose disposal. Data were analyzed using Bergman's minimal model. Parameters examined included acute insulin response to glucose, fasting insulin level, glucose disappearance constant, insulin sensitivity index, glucose effectiveness at basal insulin (SG), and glucose effectiveness at zero insulin (GEZI). Neither androgen adversely affected glucose disposal. To the contrary, treatment with ND actually improved noninsulin-mediated glucose disposal as expressed by SG and GEZI. In ND-treated men, SG (x 10(-2) min(-1)) rose from 2.4 +/- 0.2 at the end of the placebo period to 3.7 +/- 0.6 after treatment (P < 0.05), whereas GEZI (x 10(-2) min(-1)) increased from 1.8 +/- 0.2 to 3.1 +/- 0.6 (P < 0.01). We conclude that the treatment of normal men with supraphysiological doses of either TE or ND does not adversely affect glucose metabolism. Treatment with a nonaromatizable androgen, such as ND, actually improves glucose metabolism by enhancing noninsulin-mediated glucose disposal.

Adult↗
PubMed1996

Immunohistochemical localization of insulin-like growth factor binding proteins 2 and 3 in prostate tissue: clinical correlations.

PURPOSE: The insulin-like growth factor system has recently been shown to have important mitogenic effects in the prostate. The system consists of 2 ligands: insulin-like growth factor types 1 and 2, which are potent mitogens for prostate cell growth, and 6 insulin-like growth factor binding proteins that modify the activity of these growth factors. Recently, changes in serum levels of insulin-like growth factor binding proteins 2 and 3 have been identified in prostate cancer patients but in vivo studies of these changes have not been previously reported. MATERIALS AND METHODS: We performed immunohistochemical staining for insulin-like growth factor binding proteins 2 and 3 in areas of benign disease, prostatic intraepithelial neoplasia, and cancer from specimens obtained from 24 patients who underwent prostatectomy to determine changes in the quantity of these proteins with progression from the benign through the premalignant and into the malignant states. Quantification of the differences noted in the amount of insulin-like growth factor binding proteins 2 and 3 found in each of the 3 tissue types was then correlated with serum and tissue prostate specific antigen levels, pathological stage and grade of the tumors. RESULTS: Our data indicate that as human prostate tissue progresses from the benign to the malignant state, insulin-like growth factor binding protein 2 immunoreactivity in the prostatic luminal epithelial cells increases and that of insulin-like growth factor binding protein 3 decreases. Quantification of the differences noted in binding proteins 2 and 3 among all 3 tissue types was statistically significant. However, no correlation was noted between the stage or grade of prostate carcinoma and insulin-like growth factor binding protein 2 or 3 immuno-staining intensity. Additionally, no significant correlation was found between serum or tissue levels of prostate specific antigen and insulin-like growth factor binding protein 2 or 3 immunoreactivity. CONCLUSIONS: Our data suggest that significant changes in the insulin-like growth factor system occur with malignant transformation in the prostate. It is hoped that this system may eventually result in a better serum or tissue (from prostate biopsy) marker of malignant transformation, and/or represent a target for early therapeutic intervention to alter the growth and development of prostate cancer.

Humans↗
PubMed1995

Visually stimulated erection in castrated men.

Sexual interest and activity decrease following castration. We determined by objective criteria the erectile status of 16 men who were sexually active before castration for prostatic cancer. Castration was achieved by orchiectomy or hormonal manipulation. Patients answered a questionnaire regarding the medical status and erectile function before and after castration, and the blood level of testosterone was assessed. During viewing of an erotic videotape penile circumference and erection quality were monitored. Four patients (25%) achieved functional erection. Mean serum free testosterone levels in men who achieved erection were 1.125 +/- 0.362 pg./ml. (standard deviation) and 0.628 +/- 0.098 pg./ml. in those not achieving functional erection (p < 0.001). No statistically significant difference was noted in age, interval since castration, co-morbidity score or method of castration between the men who did and did not achieve erection.

Aged↗
PubMed1995

Altered growth and insulin-like growth factor-binding protein-3 production in PC3 prostate carcinoma cells stably transfected with a constitutively active androgen receptor complementary deoxyribonucleic acid.

The network of androgen-dependent growth factors regulating the growth and function of normal or neoplastic prostate epithelium is largely unknown. To facilitate studies directed at investigating this issue, androgen receptor-negative (AR-) PC3 prostate carcinoma cells were stably transfected with the expression plasmid CMV3 containing a constitutively active AR construct that is truncated at its hormone-binding domain (CMV-ARCA). The major characteristic of the resulting cell line (PC3-ARCA) was a growth rate approximately 35% slower than that of a control mock-transfected cell line (PC3-Neo). Of the several growth factors known to be present in the prostate, the current studies focused on the insulin-like growth factor (IGF) axis, specifically the IGF-binding proteins (IGFBPs), several of which are known to be abnormally produced by prostate cancer. Northern analysis showed that IGFBP-1 and -5 are not expressed by PC3-ARCA and -Neo cells. Western ligand and immunoblot analysis of medium conditioned by PC3-Neo and PC3-ARCA cells revealed that equal amounts of IGFBP-2, -4, and -6 were secreted. In contrast, IGFBP-3 was undetectable in the conditioned medium of PC3-ARCA cells, but normally produced by the AR- cell line PC3-Neo. IGFBP-3 disappearance from the conditioned medium of PC3-ARCA cells was transcriptionally regulated, as a marked decrement in IGFBP-3 messenger RNA was detected by S1 protection analysis. We investigated the responses of these cells to exogenously added IGF-I, IGF-II, or IGFBP-3. IGF-I and IGF-II stimulated the proliferation of PC3-ARCA cells, but not of PC3-Neo cells. IGFBP-3 had no effect when given alone. When IGFBP-3 was administered together with IGF-I or IGF-II, it further increased the mitogenic response observed in PC3-ARCA cells, but no effect on PC3-Neo cells was observed. In conclusion, our studies suggest that the presence of an active AR modulates the proliferation of transfected PC3 prostate cancer cells, and that this phenomenon occurs at least in part through the regulation of IGFBP-3 production.

Androgens↗
PubMed1994

Effect of 5-alpha-reductase inhibition and dexamethasone administration on the growth characteristics and intratumor androgen levels of the human prostate cancer cell line PC-3.

The endocrine treatment of metastatic prostate cancer includes castration which reliably lowers the serum testosterone (T); however, the effect on intratumor levels of T and dihydrotestosterone (DHT) is less predictable. In vitro work demonstrated that the human prostate cancer cell line PC-3 had significant 5-a-reductase activity that could be inhibited with 17b-N,N-diethylcarbamoyl-4-aza-5a-androstan-3-one (4MA). In this study, we examined the effect of 5-a-reductase inhibition with 4MA and androgen suppression with dexamethasone on the growth characteristics and intratumor androgen levels in the PC-3 cell line in male athymic nude mice (Balb/c). The mice were randomized into six treatment groups: 1) noncastrate vehicle control, 2) 4MA, 0.25 mg/day, 3) 4MA, 1 mg/day, 4) dexamethasone, 25 micrograms/day, 5) 4MA, 1 mg/day, and dexamethasone, 25 micrograms/day, and 6) castrate control group. After 21 days of treatment the animals were sacrificed, serum collected, and tumors harvested. Each treatment produced intratumor DHT levels equivalent to the castrate group. Only the low dose 4MA caused a reduction in intratumor DHT without producing castrate levels of circulating T. The combination of dexamethasone and 4MA was less effective in lowering the intratumor DHT/T ratio than 4MA alone. No significant differences in tumor growth parameters were noted between intact control animals and any of the treatment arms. Serum T levels correlated poorly with intratumor androgen levels. Five-a-reductase inhibition produced castrate levels of intratumor DHT in the nonandrogen-dependent prostate cancer cell line PC-3. The combination of dexamethasone and 5-a-reductase inhibition with 4MA appears to be less effective in lowering intratumor androgen levels than either therapy alone.

5-alpha Reductase Inhibitors↗
PubMed1994

Insulin-like growth factor-binding protein-3 expression and secretion by cultures of human prostate epithelial cells and stromal fibroblasts.

Prostate-specific antigen (PSA) was recently shown to be an insulin-like growth factor-binding protein (IGFBP)-3 protease. However, only IGFBPs-2 and -4 have been identified in conditioned medium of prostate epithelial cells. Using cultures of human prostate epithelial and stromal fibroblastic cells, we examined conditioned medium and cell extracts for evidence of IGFBP-3 expression and secretion. Western ligand blotting of conditioned medium from epithelial or stromal cultures revealed the presence of IGFBPs in the molecular weight range 36-48 kDa, suggestive of IGFBP-3. Western immunoblots of these media confirmed the presence of IGFBP-3. Northern analyses of extracts of both stromal and epithelial cells showed a 2.5 kb band, the size of IGFBP-3 mRNA. We conclude that prostate cells express IGFBP-3 and that local proteolysis by PSA could modify this binding protein's actions in the prostate.

Blotting, Northern↗
PubMed1993

Relationship of insulin secretory pulses to sex hormone-binding globulin in normal men.

Insulin has emerged as a regulator of sex hormone-binding globulin (SHBG) production in vitro and in vivo. A role for insulin in regulating SHBG exists in insulin resistant states such as obesity and polycystic ovary syndrome. The relationship of in vivo insulin secretion rates to SHBG levels in healthy normal men is less well documented. Hepatic synthesis of SHBG may be influenced by quantitative insulin exposure as well as qualitative characteristics such as frequency and amplitude of insulin secretory pulses. The present study was undertaken to assess these relationships in 10 normal men. Adiposity was determined by the body mass index and fat distribution by the waist hip ratio. Peripheral insulin sensitivity was determined by the euglycemic clamp technique at an insulin infusion rate of 287 pmol/min.m2. SHBG levels were determined in the fasting state by RIA. Arterialized venous samples for C-peptide were obtained every 2 min for 90 min in the basal state. Individual C-peptide kinetics were derived after a bolus injection of biosynthetic human C-peptide and a previously validated two compartmental model. Insulin secretion rates at each time point were calculated using the plasma C-peptide values and the C-peptide kinetics. Insulin secretion rates were unrelated to SHBG concentrations (r = -0.29, P > 0.05). The insulin secretory pulse interval had a significant positive association with SHBG levels (r = 0.86, P < 0.05). Insulin secretory pulse amplitude, body mass index, waist hip ratio, and peripheral insulin sensitivity were not associated with SHBG concentrations in a regression analysis. We postulate that insulin secretory pulse frequency may be an important determinant of SHBG synthesis in normal man.

Adipose Tissue↗
PubMed1993

Testosterone administration increases insulin-like growth factor-I levels in normal men.

Although testosterone (T) administration can increase insulin-like growth factor-I (IGF-I) when administered to hypogonadal men, no studies have examined whether this occurs in normal men. The present study was undertaken to determine if an increase in IGF-I may be part of the anabolic effect of androgens. We enrolled 11 normal men in a randomized, double-blinded cross-over study. Subjects were assigned to receive either T enanthate (TE) (300 mg im, each week) or nandrolone (ND) decanoate (300 mg im, each week) for 6 weeks. After a washout period subjects were administered the alternate treatment. Pre- and posttreatment serum was analyzed for IGF-I by RIA after acid-ethanol extraction. Results expressed as mean +/- SEM (Table 1). IGF-binding protein-3 was measured by RIA and was unchanged in the TE treatment and decreased significantly after ND treatment. Although GH levels were not significantly different after either TE or ND treatment, they tended to increase after TE treatment (1.23 +/- 0.28 ng/mL vs. 3.3 +/- 1.03 ng/mL) but remained unchanged after ND treatment (1.68 +/- 0.68 ng/mL vs. 1.89 +/- 0.64 ng/mL). Serum total T levels increased 32 +/- 0.05 nmol/L in the TE-treated men, but fell by 7 +/- 0.02 nmol/L in the ND-treated men (P < 0.0001). Serum estradiol levels rose by 193.04 +/- 19.82 pmol/L in the TE-treated men although falling by 50.65 +/- 34.50 pmol/L in the ND-treated men (P < 0.0002). These data indicate that when normal men are given TE, serum IGF-I levels increase after 6 weeks of treatment. Treatment with ND did not change serum levels of IGF-I but did decrease the level of the major serum IGF-BP and therefore the level of bioavailable IGF-I may be increased in the ND group.

Adult↗
PubMed1992

The effects of sex hormone binding globulin (SHBG) on testosterone transport into the cerebrospinal fluid.

The movement of testosterone (T) from blood across the blood-brain barrier (BBB) is thought to reflect the combined effects of T's lipid solubility and the presence of circulating binding proteins for T such as albumin or sex hormone binding globulin (SHBG). Since the adult rat lacks a circulating specific high affinity sex steroid binding protein, examination of the disappearance from serum and uptake into cerebrospinal fluid (CSF) of [3H]T before and after SHBG or albumin infusion should provide insight into the function of these two proteins with respect T transport. Three groups of adult male Sprague-Dawley rats were cannulated at the femoral vein and cisterna magna. In a control group (n = 8), [3H]T was given as an intravenous bolus beginning at time zero; multiple serum and CSF collections were assayed for counts per min (cpm) during the subsequent 45 min. Data from these animals were then compared to those seen in animals that received either purified human SHBG (hSHBG) (n = 7) or human albumin (hALB) (n = 6) 10 min prior to the [3H]T infusion. High performance liquid chromatography was used to monitor the metabolic fate of the steroid infusate at the end of each study period. Infusion of hSHBG increased serum concentrations from undetectable to 93.8 nM/l (mean +/- SEM, n = 6). Administration of hALB significantly increased (25.0 +/- 1.2 g/l at baseline, 33.4 +/- 1.6 g/l post-infusion, mean +/- SEM, P less than 0.03, n = 5) the circulating albumin concentration. Comparison of data from each group of animals demonstrated that (1) following an i.v. injection of radiolabeled T, the initial decline in serum [3H]T was significantly reduced (P less than 0.03) in the presence of hSHBG, (2) hALB did not affect the movement of [3H]T out of serum, (3) the time to peak appearance of [3H]T in the CSF was significantly delayed (P less than 0.02) by the presence of circulating hSHBG, and (4) the net quantity of [3H]T found in the cSF under steady-state conditions was not affected by serum SHBG or albumin levels. This study demonstrates that high-affinity steroid binding proteins do modulate the transport of sex steroids across the BBB. Specifically, SHBG delays the clearance of T from serum and slows the rate of T uptake into the CSF during non-equilibrium conditions.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗
PubMed1992

Relationship of serum inhibin levels to serum follicle stimulating hormone and sperm production in normal men and men with varicoceles.

The purpose of this study was to examine the relationships between serum inhibin levels as measured by RIA and serum FSH and sperm concentration. Three groups of men were used for this study: group I, normal fertile men (n = 67); group II, fertile men with a varicocele (n = 57); and group III, infertile men with a varicocele (n = 21). There were no differences in mean serum inhibin levels between the three groups. The two groups of men with varicoceles exhibited higher serum FSH levels and FSH responses to GnRH than the normal men. Sperm counts in both groups II and III were significantly lower than group I. In the normal men there was an inverse correlation between baseline serum inhibin and serum FSH levels and GnRH stimulated FSH levels, r = -0.415 and 0.422, P less than 0.005, respectively. Furthermore, the normal men exhibited a positive correlation between serum inhibin measurements and sperm concentration and testicular volume, r = 0.35 and 0.26, P less than 0.01 and less than 0.05, respectively. In neither group of men with a varicocele were these relationships found. These data demonstrate that serum inhibin does correlate with FSH in a negative fashion, when the reproductive system is normal, as would be expected for a negative feedback factor. Finally, the relationship of serum inhibin levels to testicular size and sperm count in the normal men suggests that serum inhibin levels reflect to some extent the integrity of seminiferous tubule function.

Follicle Stimulating Hormone↗
PubMed1991

Psychological and serum homovanillic acid changes in men administered androgenic steroids.

We report a difference in the response of serum homovanillic acid (HVA) and in the performance of some psychological tasks before and after the administration of testosterone enanthate (TE, 100 or 300 mg/wk) or nandrolone decanoate (ND, 100 or 300 mg/wk) for 6 wk to healthy men. Serum HVA was significantly increased in both the low- and high-dose ND groups, from 8.4 +/- 1.0 and 8.7 +/- 0.5 pmol/ml (mean +/- SE) to 11.6 +/- 1.7 and 10.7 +/- 1.1 pmol/ml respectively. No significant changes in HVA were observed for the groups administered TE, nor in 5-HIAA for any of the groups. The influence of ND on the dopaminergic system, which is reflected in increased serum HVA, appears to be independent from the psychological effects which were produced by both androgens. The only change in psychomotor test performance was an improvement in the first trial of a pegboard task. All subjects except those receiving ND (100 mg/wk) were significantly more optimistic in the prediction of their own performance for all nondominant hand tasks (pegboard and finger tapping). The "hostility" and "resentment and aggression" subscales of the MMPI increased significantly in all groups, more so in the high-dose groups.

Adult↗