Different Testosterone and LH Relationships in Infertile Men

Morrow, Anthony; Baker, H. W. G.; Burger, Henry

doi:10.1002/j.1939-4640.1986.tb00937.x

Cited by 15 publications

(15 citation statements)

References 14 publications

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“…Dysfunction of Sertoli cells, including inhibin secretion, might in turn cause increased levels of FSH. Furthermore, positive correlation between the FSH and LH levels of males has been reported [21,22], since secretion of these gonadotropins shares a common regulatory system. Taken together, the hyperplasia of Leydig cells in the repro22/repro22 mouse might be caused by dysfunction of Sertoli cells that results in elevated secretion of both FSH and LH; however, measurement of the FSH, LH and inhibin levels in mutant mice is necessary to prove this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

et al. 2008

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Abstract.Repro22 is an N-ethyl-N-nitrosourea (ENU)-induced mutation in mice showing depletion of both male and female germ cells. In the present study, we investigated the male phenotypes of the mutant mouse at the adult stage. The repro22/repro22 homozygous mice showed reduced body weights as well as markedly reduced testis weights. Histological examination of the testes at 4 and 10 months of age showed no germ cells in the seminiferous tubules of the affected testis while a number of Sertoli cells were observed in the tubules. In addition to the germ cell depletion, the testes of the affected mouse contained expanded intertubular spaces that were filled by Leydig cell-like interstitial cells. These interstitial cells were confirmed to be Leydig cells by immunohistochmical staining using anti-3β-HSD antibody. The estimated number of Leydig cells in the affected testes at 10 months of age increased approximately 2 fold compared with those of normal testes. Furthermore, the plasma testosterone levels of the affected mice at 10 months of age were significantly higher than those of the normal mice. These findings indicated that the repro22/repro22 mouse developed hyperplasia of Leydig cells that was presumably caused by the absence of germ cells in the seminiferous tubules. Key words: ENU mutagenesis, Germ cell, Infertility, Leydig cell, Mouse, Testosterone (J. Reprod. Dev. 54: [225][226][227][228] 2008) nfertility is a major health problem worldwide that influences more than 10% of couples, and approximately 50% of cases of infertility are caused by male factors. In particular, Sertoli cellonly syndrome, a form of non-obstructive azoospermia, is the most serious male infertility, as patients with this disorder show germ cell depletion and are untreatable using assisted reproduction techniques. Although a significant portion of male infertilities is believed to be caused by autosomal recessive mutations [1], the genetic factors that underlay most nonsyndromic male infertilities have not yet been identified, with a few exceptions [2,3]. Mutant mice established by gene targeting technology, chemical mutagenesis and spontaneous mutations [4][5][6][7], showing various features of infertility are expected to be useful animal models for investigating the pathogenesis and genetic factors of human infertilities. However, only a limited number of mouse models for Sertoli cell-only syndrome or germ cell depletion have been reported [8][9][10][11]. Repro22 is a mutation in mice recently produced by N-ethyl-Nnitrosourea (ENU)-induced mutagenesis at The Jackson Laboratory, showing depletion of germ cells in both the male and female. In the present study, we investigated male phenotypes of the mutant mouse at the adult stage and found that the mutant mouse showed Leydig cell hyperplasia and an elevated plasma testosterone level in addition to germ cell depletion. Materials and MethodsThe mice bearing the repro22 mutation were produced and provided by the ReproGenomics Program at The Jackson Laboratory. The mice have a mixed g...

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Section: Discussionmentioning

confidence: 99%

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

et al. 2008

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“…Testosterone A solid-phase assay incorporating l25I-labelled testos¬ terone was employed. The interassay variations were 5-2 and 7-2% at concentrations of 8-8 and 19-5 nmol/1 (Morrow, Baker & Burger, 1986). The normal range for testosterone was 10-40 nmol/1.…”

Section: Inhibinmentioning

confidence: 97%

Serum inhibin levels in normal men and men with testicular disorders

Kretser

McLachlan

Robertson

et al. 1989

Journal of Endocrinology

113

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Serum concentrations of inhibin, FSH and LH were measured in 39 normal men and 127 men with testicular disorders resulting in infertility. The infertile men were divided into groups on the basis of their mean sperm count, FSH levels and karyotype. The mean (+/- S.D) serum concentrations of inhibin in the normal men was 554 +/- 156 U/l and did not differ significantly from those groups with oligospermia, azoospermia or Klinefelter's syndrome. Combined analyses of all groups did not reveal any significant correlation between serum concentrations of inhibin and FSH or with any other parameter measured. Serum concentrations of FSH and LH were positively correlated, and Leydig cell dysfunction, as evidenced by increased serum LH levels, low testosterone levels or a declining testosterone/LH ratio were found with severe spermatogenic damage. The failure of serum concentrations of inhibin to correlate with those of FSH levels or the degree of testicular damage raise questions as to the clinical value of this parameter alone.

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“…Morrow et al (24) reported comparable findings with a positive correlation between LH and testosterone in infertile men with low FSH values compared to those with high FSH levels, in whom the correlation was negative, suggesting heterogeneous causes for testicular malfunction. Interestingly, the group of patients with low inhibin B but normal FSH levels had significantly lower LH values in the presence of normal testosterone compared to other patients with a reduction in inhibin B levels.…”

Section: Discussionmentioning

confidence: 80%

Serum Inhibin B in Combination with Serum Follicle-Stimulating Hormone (FSH) Is a More Sensitive Marker Than Serum FSH Alone for Impaired Spermatogenesis in Men, But Cannot Predict the Presence of Sperm in Testicular Tissue Samples¹

Eckardstein¹,

Simoni²,

Bergmann³

et al. 1999

The Journal of Clinical Endocrinology & Metabolism

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The measurement of serum FSH is useful in the diagnostic workup of the infertile male, but fails to predict the presence of sperm in testicular tissue. We investigated whether inhibin B reflects testicular morphology and the presence of sperm more accurately than FSH. Serum inhibin B and gonadotropin levels were determined in 91 infertile men undergoing diagnostic bilateral testicular biopsy. In 52 of the 91 patients multiple samples were taken for testicular sperm extraction (TESE). Inhibin B levels were (mean +/- SEM) 238+/-32 pg/mL in men with normal spermatogenesis (n = 9), 102+/-18 pg/mL in men with spermatogenetic arrest (n = 15), 98+/-16 pg/mL in hypospermatogenesis (n = 23), 41+/-6 pg/mL in focal Sertoli cell-only syndrome (SCO; n = 26), and 27+/-8 pg/mL in complete SCO (n = 18). The percentage of SCO tubuli was more strongly correlated to serum inhibin B (r = -0.58; P<0.01) than to FSH (r = 0.34; P<0.05). Similarly, the percentage of tubules with elongated spermatids was significantly (P<0.05) more strongly correlated to serum inhibin B (r = 0.65; P<0.01) than to FSH (r = -0.4; P<0.01). Thus, inhibin B is slightly more sensitive than FSH as an index of the spermatogenic status. Neither FSH nor inhibin B alone, however, could predict the type of spermatogenetic damage exactly. The combination of FSH and inhibin B had high diagnostic sensitivity (88%) and specificity (83%) for the presence of elongated spermatids in testicular biopsies. Sperm could be retrieved in 34 (65%) of the TESE patients. The combination of inhibin B and FSH measurement showed a sensitivity of 75% and a specificity of 73% when identifying patients in whom sperm could possibly be retrieved by TESE. We conclude that although the measurement of serum inhibin B improves the sensitivity of predictive tests for the presence of sperm in histology or for TESE, this parameter cannot accurately predict TESE outcome.

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Different Testosterone and LH Relationships in Infertile Men

Cited by 15 publications

References 14 publications

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

Serum inhibin levels in normal men and men with testicular disorders

Serum Inhibin B in Combination with Serum Follicle-Stimulating Hormone (FSH) Is a More Sensitive Marker Than Serum FSH Alone for Impaired Spermatogenesis in Men, But Cannot Predict the Presence of Sperm in Testicular Tissue Samples¹

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Different Testosterone and LH Relationships in Infertile Men

Cited by 15 publications

References 14 publications

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

Leydig Cell Hyperplasia in an ENU-induced Mutant Mouse with Germ Cell Depletion

Serum inhibin levels in normal men and men with testicular disorders

Serum Inhibin B in Combination with Serum Follicle-Stimulating Hormone (FSH) Is a More Sensitive Marker Than Serum FSH Alone for Impaired Spermatogenesis in Men, But Cannot Predict the Presence of Sperm in Testicular Tissue Samples1

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Serum Inhibin B in Combination with Serum Follicle-Stimulating Hormone (FSH) Is a More Sensitive Marker Than Serum FSH Alone for Impaired Spermatogenesis in Men, But Cannot Predict the Presence of Sperm in Testicular Tissue Samples¹