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  1. #1
    Senior Bodybuilder sok's Avatar
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    Ρέθυμνο, Greece.

    Default Τα Cortisol Inhibitors μειώνουν την testo;

    Ψάχνοντας για το Lean Xtreme (Cortisol Inhibitor) έπεσα πάνω σε αυτές τις έρευνες.
    Αν κάποιος έχει κάτι πάνω σε αυτό ή προσωπική εμπειρία παρακαλώ ας γράψει.

    Δεν κάνω μετάφραση γιατί φοβάμαι μην παρερμηνεύσω κάτι και φανεί λάθος το συμπέρασμα.

    We have proposed that the 11?-hydroxysteroid dehydrogenase (11?-HSD) of Leydig cells protects against glucocorticoid-induced inhibition of testosterone (T) production. However, Leydig cells express type I 11?-HSD, which has been shown to be reductive in liver parenchymal cells. Because reduction would have the opposite effect of activating glucocorticoid, the present study was designed to determine: 1) whether Leydig cell 11?-HSD is primarily oxidative or reductive; and 2) whether oxidative and reductive activities are separately modified by known regulators of Leydig cell steroidogenic function. Leydig cells and liver parenchymal cells were purified from mature male Sprague-Dawley rats (250 g BW), and 11?-HSD oxidative and reductive activities were measured using radiolabeled substrates and TLC of triplicate media samples from 1-h incubations immediately after cell isolation. Enzyme activities also were examined in purified Leydig cells at the end of 3 days of culture in vitro in the presence of LH (10 ng/ml), dexamethasone (DEX, 100 nM), T (50 nM), or epidermal growth factor (EGF, 50 ng/ml). In confirmation of previous reports, the reductive activity of 11?-HSD was predominant over oxidation in liver parenchymal cells. In contrast, 11?-HSD oxidative activity prevailed over reduction in Leydig cells by a ratio of 2:1. The activities of 11?-HSD also were analyzed in Leydig cells that were purified 7 days after endogenous glucocorticoid levels were suppressed by adrenalectomy (ADX). Oxidative activity declined in Leydig cells after ADX (22.53 ± 1.12 pmol/h·106 cells, mean ± SEM vs. 31.47 ± 1.48 pmol/h·106 cells in sham-operated controls, P < 0.05), whereas there was no change in reductive activity. This indicated that physiologically active corticosterone is involved in maintaining the predominance of 11?-HSD oxidation. When enzyme activities were analyzed in Leydig cells after 3 days of hormonal treatment in vitro, oxidation and reduction were observed to change in opposing directions. Culture of Leydig cells from sham-operated control rats with either LH, T, or EGF resulted in declines in oxidative activity from 33.35 ± 0.77 to 28.24 ± 1.93, 27.30 ± 0.96, and 24.13 ± 1.02 pmol/h·106 cells ( ± SE), respectively. However, EGF stimulated 11?-HSD reductive activity in cultured Leydig cells from both control (from 18.97 ± 1.10 to 27.16 ± 0.71 pmol/h·106 cells and ADX rats (from 16.51 ± 0.75 to 23.56 ± 0.84 pmol/h·106 cells). Among the hormonal treatments, only DEX increased oxidative activity and simultaneously decreased reductive activity in Leydig cells from ADX rats. This increase accentuated the predominance of oxidative activity in Leydig cells, with a ratio of oxidative to reductive activity of 4:1 after DEX treatment, compared with 2:1 in controls that were untreated. We conclude that 11?-HSD activity in Leydig cells is primarily oxidative. Moreover, oxidation and reduction are regulated separately by hormones.

    Πηγή: http://endo.endojournals.org/cgi/content/abstract/138/1/156?ijkey=6e819c29f13ec9e42ea827f94f83f1dc9ae07594&keytype2=tf_ipsecsha

    It has been shown that stress or disease-induced increases in plasma corticosterone result in diminished testosterone secretion from the testes. This article reviews investigations from our laboratories that explore the role of 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) in this process. It is proposed that the level of 11 beta-OHSD in Leydig cells dictates the level of intracellular glucocorticoid available to the glucocorticoid receptor and thus the potency of corticosteroid as an inhibitor of testosterone secretion. Stressed and unstressed rats were housed under simulated natural conditions in a Visible Burrow System. Stressed animals showed elevated plasma corticosteroid, lowered plasma testosterone, and diminished testicular 11 beta-OHSD, Immunocytochemical analysis showed that only Leydig cells of the rat testis contain 11 beta-OHSD and glucocorticoid receptors. Half-maximal inhibition of testosterone by Leydig cells required 1.5 nM dexamethasone or 0.4 microM corticosterone. Glycyrrhetinic acid, an inhibitor of 11 beta-OHSD, increased the potency of corticosterone, but did not affect dexamethasone based inhibition. The glucocorticoid receptor blocker, RU 486, prevented inhibition by both corticosterone and dexamethasone. Other classes of steroid were not inhibitors of testosterone biosynthesis. Thus, 11 beta-OHSD oxidizes corticosterone to the inactive metabolite 11-dehydrocorticosterone, relieving steroid-dependent inhibition of Leydig cell function. Lowered enzyme activity increases glucocorticoid dependent inhibition of testosterone production. We conclude that the evidence supports a role of 11 beta-OHSD in testosterone secretion by the testes.

    Πηγή: http://www.ncbi.nlm.nih.gov/pubmed/8191550?dopt=Abstract

    The paper from M. P. Hardy?s laboratory in this issue of Endocrinology addresses the ontogeny of 11-HSD oxidase and reductase activity and modulation of glucocorticoid action upon testosterone synthesis in Leydig cells (12). Elevations in circulating levels of glucocorticoids depress testosterone production by mature Leydig cells, resulting in decreased serum testosterone levels (13) and the elimination of endogenous corticosterone levels in vivo increases the steroidogenic capacity of purified Leydig cells in vitro. The demonstration of 11-HSD-1 messenger RNA and protein in Leydig cells led to the hypothesis that this isozyme regulates steroidogenesis in the testes by inactivating glucocorticoids within the cell, allowing normal testosterone synthesis (14).
    Adult Leydig cells have both oxidative and reductive 11-HSD activity with oxidation prevailing over reduction.

    Πηγή: http://endo.endojournals.org/cgi/content/short/138/12/5087

    Sharp reductions in immunocytochemical staining intensity were observed in the treated animals for a Leydig cell marker, 11?-hydroxysteroid dehydrogenase, which occurred concurrently with decreased serum T levels. This was consistent with the hypothesis that CORT-mediated induction of apoptosis leads to declines in Leydig cell numbers, thereby affecting T production. These results suggest that excessive exposure to CORT initiates apoptosis in rat Leydig cells, potentially contributing to suppression of circulating T levels during stress and other conditions in which glucocorticoid concentrations are elevated.

    Πηγή: http://endo.endojournals.org/cgi/content/abstract/143/1/130

    Μετά βρήκα και αυτή που ψιλοαναιρεί τις παραπάνω.

    (1)Safety and pharmacokinetic study with escalating doses of 3-acetyl-7-oxo-dehydroepiandrosterone in healthy male volunteers.

    Davidson M, Marwah A, Sawchuk RJ, Maki K, Marwah P, Weeks C, Lardy H.

    Chicago Center for Clinical Research, Ill, USA.

    OBJECTIVES: To evaluate the safety and pharmacokinetics of 3-acetyl-7-oxo-DHEA (3beta-acetoxyandrost-5-ene-7,17-dione) given orally. DESIGN: A randomized, double blind, placebo-controlled, escalating dose study. SETTING: The Chicago Center for Clinical Research. PARTICIPANTS: Twenty-two healthy men. STUDY METHOD: The participants received placebo (n = 6) or 3-acetyl-7-oxo-DHEA (n = 16) at 50 mg/d for 7 days followed by a 7-day washout; 100 mg/d for 7 days followed by a 7-day washout; and 200 mg/d for 28 days. OUTCOME MEASURES: Safety parameters, evaluated at each dose level, included measurement of total testosterone, free testosterone, dihydrotestosterone, estradiol, cortisol, thyroxin and insulin levels. Analyses for 7-oxo-DHEA-3beta-sulfate (DHEA-S), the only detectable metabolic product of the administered steroid, were conducted on plasma drawn from all subjects at 0.25, 0.5, 1, 2, 4, 6 and 12 hours after the final 100 mg dose of 3beta-acetyl-7-oxo-DHEA. RESULTS: There were no differences in the clinical laboratory values or in reported minor adverse experiences, between treatment and placebo groups. In general, blood hormone concentrations were unaffected by the treatment with 3beta-acetyl-7-oxo-DHEA and remained within the normal range. No changes in vital signs, blood chemistry or urinalysis occurred during treatment with 3beta-acetyl-7-oxo-DHEA compared to placebo. The administered steroid was not detected in the blood but was rapidly converted to 7-oxo-DHEA-S, the concentrations of which were proportional to dose. This steroid sulfate did not accumulate; plasma concentrations 12 hours after the 3beta-acetyl-7-oxo-DHEA dose at 7 and 28 days on the 200 mg/d dose were 15.8 and 16.3 microg/L respectively. The mean time to peak plasma level of 7-oxo-DHEA-S was 2.2 hours; the mean half life was 2.17 hours. The apparent clearance averaged 172 L/h, and the apparent mean volume of distribution was 540 L. CONCLUSION: These results indicate that 3beta-acetyl-7-oxo-DHEA is safe and well tolerated in normal healthy men at doses up to 200 mg/d for 4 weeks.

    Πηγή: http://www.ncbi.nlm.nih.gov/pubmed/11055323
    Last edited by sok; 30-04-10 at 21:04.

  2. #2
    Senior Bodybuilder
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    αυτα τα αρθρα τα διαβαζα κ εγω προχτες.απ οτι εχω καταλαβει φιλε μου προκειται για ενα πολυ αμφιλεγομενο θεμα με απειρες ερευνες και συζητησεις..λογικα οι πιο παλιοι θα μπορεσουν να μας βοηθησουν!!

  3. #3
    Senior Bodybuilder sok's Avatar
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    Ρέθυμνο, Greece.


    Να προσθέσω και αυτή για το forskolin το οποίο υπάρχει στο LX και φέρνει σε ισορροπία την κατάσταση.

    OBJECTIVE: This study examined the effect of forskolin on body composition, testosterone, metabolic rate, and blood pressure in overweight and obese (BMI > or = 26 kg/m(2)) men. RESEARCH METHODS AND PROCEDURE: Thirty subjects (forskolin, n = 15; placebo, n = 15) were studied in a randomized, double-blind, placebo-controlled study for 12 weeks. RESULTS: Forskolin was shown to elicit favorable changes in body composition by significantly decreasing body fat percentage (BF%) and fat mass (FM) as determined by DXA compared with the placebo group (p < or = 0.05). Additionally, forskolin administration resulted in a change in bone mass for the 12-week trial compared with the placebo group (p < or = 0.05). There was a trend toward a significant increase for lean body mass in the forskolin group compared with the placebo group (p = 0.097). Serum free testosterone levels were significantly increased in the forskolin group compared with the placebo group (p < or = 0.05). The actual change in serum total testosterone concentration was not significantly different among groups, but it increased 16.77 +/- 33.77% in the forskolin group compared with a decrease of 1.08 +/- 18.35% in the placebo group. DISCUSSION: Oral ingestion of forskolin (250 mg of 10% forskolin extract twice a day) for a 12-week period was shown to favorably alter body composition while concurrently increasing bone mass and serum free testosterone levels in overweight and obese men. The results indicate that forskolin is a possible therapeutic agent for the management and treatment of obesity.

    Πηγή: http://www.ncbi.nlm.nih.gov/pubmed/16129715
    Last edited by sok; 01-05-10 at 04:13.


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