Reduction of Serum Testosterone in Men by Licorice

Armanini, Decio; Bonanni, Guglielmo; Palermo, Mario

doi:10.1056/nejm199910073411515

Cited by 80 publications

(47 citation statements)

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“…Interestingly, however, Sakamoto & Wakabayashi [30] showed that oral administration of a Kanzo preparation, glycyrrhizin or glycyrrhetinic acid decreased in vitro testosterone production in Leydig cells of rats stimulated by luteinizing hormone. The testosterone-reducing effect of glycyrrhizin and glycyrrhetinic acid was observed in female rats [37,38], but not in males [the present study], and there is controversy over the influence of licorice in men [1,2,16,25]. It is hypothesized that, in spite of partial suppression of the basal production of testosterone following the inhibition of steroid-metabolizing enzymes by licorice, production of testosterone stimulated by luteinizing hormone is significantly blocked in the testes, or in the ovaries in the proestrous cycle [3,6,18,30,37,38,44].…”

Section: Discussionmentioning

confidence: 70%

“…This testosterone-lowering effect was also experimentally confirmed in ovarian culture of licorice-treated female rats [37,38]. Therefore, it was proposed that licorice could cause the deficiency of serum testosterone, leading to sexual dysfunction or decline of libido in men [1,2]. However, the testosterone-reducing effect of licorice in males is controversial, since the results of Armanini et al [1,2] have not been reproduced by other investigators [16,25].…”

Section: Discussionmentioning

confidence: 96%

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Licorice Extract Does Not Impair the Male Reproductive Function of Rats

Shin¹,

Jang²,

Choi³

et al. 2008

Exp. Anim.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 96%

Licorice Extract Does Not Impair the Male Reproductive Function of Rats

Shin¹,

Jang²,

Choi³

et al. 2008

Exp. Anim.

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“…30 A description of the main drugs, respective doses, potential drug interactions and side effects can be found in Table 2. [13][14][15][16][17][18][19][20]23,24,27,[30][31][32][33][34][35][36][37][38] DISCUSSION Sexual performance among patients with schizophrenia may differ from the qualitative and quantitative patterns in the normal population. It may be altered through three main factors: by the disease itself as a consequence of affective and/or cognitive impairment; by antipsychotic drugs; and by other clinical problems (such as diabetes, hypertension, alcohol and drug abuse).…”

Section: Resultsmentioning

confidence: 99%

“…The mechanism is unknown: either a direct inhibitory effect on prolactin release from the pituitary or an indirect action via a reduction in estradiol, or both 24,28 Nausea, pseudo-hyperaldosteronism, 37 myoglobinuria (rare); long term effect: may decrease serum testosterone levels, 38 use is not recommended for pregnant women or for people with liver and kidney disorders 37 No psychiatric drug interactions known Thiazide diuretics: increased potassium loss; digitalis: more sensitivity to digitalis due to hypokalemia Sildenafi l 50 mg/week Phosphodiesterase inhibitor [20][21][22][23] Flushing (4-10%), dizziness (2%), headache (11-16%), diarrhea (4%), dyspepsia (4-8%), abnormal vision, nasal congestion, skin rash (2%), myocardial infarction (rare), priapism (rare)…”

Section: G Three Times Dailymentioning

confidence: 99%

A systematic review on clinical management of antipsychotic-induced sexual dysfunction in schizophrenia

2006

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INTRODUCTION: Sexual dysfunction frequently occurs in patients with schizophrenia under antipsychotic therapy, and the presence of sexual side effects may affect compliance. The aim of this study was to review and describe clinical findings relating to the appropriate management of such dysfunctions. MATERIAL AND METHODS: The research was carried out through Medline (from 1966 to March 2005), PsycInfo (from 1974 to March 2005), and Cochrane Library (from 1965 to March 2005) and included any kind of study, from case reports to randomized trials. RESULTS: The most common sexual dysfunctions found in the literature were libido decrease, difficulties in achieving and maintaining erection, ejaculatory dysfunction, orgasmic dysfunction, and menstrual irregularities. Thirteen papers were found: eight of them were open-label studies, four were descriptions of cases, and only one was a randomized clinical trial. All of them were short-term and had small sample sizes. The agents used were: bromocriptine, cabergoline, cyproheptadine, amantadine, shakuyaku-kanzo-to, sildenafil and selegiline. DISCUSSION: There was no evidence that those agents had proper efficacy in treating the antipsychotic-induced sexual dysfunction. An algorithm for managing sexual dysfunction induced by antipsychotics is suggested as a support for clinical decisions. Since the outcome from schizophrenia treatment is strongly related to compliance with the antipsychotics, prevention of sexual dysfunction is better than its treatment, since there is a scarcity of data available regarding the efficacy of intervention to deal with these problems.

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“…When testicular 11␤HSD is inhibited, excessive glucocorticoid action suppresses testosterone production in Leydig cells (Monder et al, 1994a). In particular, men who ingest the 11␤HSD inhibitor glycyrrhetinic acid in licorice, have reduced serum testosterone levels (Armanini et al, 1999). To date, two distinct forms of 11␤HSD have been identified: type I 11␤HSD (11␤HSD-I), which was first purified from rat liver and later cloned, has both oxidative and reductive activities (Lakshmi and Monder, 1988;Agarwal et al, 1989); and Type II 11␤HSD (11␤HSD-II), first identified in kidney and later cloned, is exclusively oxidative with a high affinity for glucocorticoids (Rusvai and Naray-FejesToth, 1993;Albiston et al, 1994;Zhou et al, 1995).…”

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confidence: 99%

Protein Kinase C Increases 11β‐Hydroxysteroid Dehydrogenase Oxidation and Inhibits Reduction in Rat Leydig Cells

Hardy

2002

Journal of Andrology

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ABSTRACT:Glucocorticoid hormone controls Leydig cell steroidogenic function through a receptor-mediated mechanism. The enzyme 11␤-hydroxysteroid dehydrogenase (11␤HSD) plays an important role in Leydig cells by metabolizing glucocorticoids, and catalyzing the interconversion of corticosterone (the active form in rodents) and 11-dehydrocorticosterone (the biologically inert form). The net direction of this interconversion determines the amount of biologically active ligand, corticosterone, available for glucocorticoid receptor binding. We hypothesize that 11␤HSD oxidative and reductive activities are controlled separately in Leydig cells, and that shifts in the favored direction of 11␤HSD catalysis provide a mechanism for the control of intracellular corticosterone levels. Therefore, in the present study, we tested the dependency of 11␤HSD oxidative and reductive activities on protein kinase C (PKC) and calcium-dependent signaling pathways. 11␤HSD oxidative and reductive activities were measured in freshly isolated intact rat Leydig cells using 25 nM radiolabeled substrates after treatment with protein kinase modulators. We found that PKC and calcium-dependent signaling had opposing effects on 11␤HSD oxidative and reductive activities. Stimulation of PKC using the PKC activator, 6-[N-decylamino]-4-hydroxymethylinole (DHI), increased 11␤HSD oxidative activity from a conversion rate of 5.08% to 48.23%with an EC 50 of 1.70 Ϯ 0.44 M (mean Ϯ SEM), and inhibited reductive activity from 26.90% to 3.66% conversion with an IC 50 of 0.22 Ϯ 0.05 M. This indicated that PKC activation in Leydig cells favors 11␤HSD oxidation and lower levels of corticosterone. The action of DHI was abolished by the PKC inhibitor bisindolylmaleimide I. In contrast, addition of calcium to Leydig cells increased 11␤HSD reductive activity while decreasing oxidative activity, thereby favoring reduction and conversion of inert 11-dehydrocorticosterone into active corticosterone. The opposite effect was seen after elimination of calciumdependent signaling, including removal of calcium by EGTA or addition of the calmodulin (calcium binding protein) inhibitor SKF7171A, or the calcium/calmodulin-dependent protein kinase I (CaMK II) inhibitor, KN62. We conclude that 11␤HSD oxidative and reductive activities are separately regulated and that, in contrast to calcium-dependent signaling, PKC stimulates 11␤HSD oxidation while inhibiting 11␤HSD reduction. Maintenance of a predominantly oxidative 11␤HSD could serve to eliminate adverse glucocorticoid-induced action in Leydig cells.

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Reduction of Serum Testosterone in Men by Licorice

Cited by 80 publications

References 3 publications

Licorice Extract Does Not Impair the Male Reproductive Function of Rats

Licorice Extract Does Not Impair the Male Reproductive Function of Rats

A systematic review on clinical management of antipsychotic-induced sexual dysfunction in schizophrenia

Protein Kinase C Increases 11β‐Hydroxysteroid Dehydrogenase Oxidation and Inhibits Reduction in Rat Leydig Cells

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