scholarly journals Impaired Leydig Cell Function in Infertile Men: A Study of 357 Idiopathic Infertile Men and 318 Proven Fertile Controls

2004 ◽  
Vol 89 (7) ◽  
pp. 3161-3167 ◽  
Author(s):  
A.-M. Andersson ◽  
N. Jørgensen ◽  
L. Frydelund-Larsen ◽  
E. Rajpert-De Meyts ◽  
N. E. Skakkebæk
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Infant Development ◽  
Cell Function ◽  
Serum Testosterone ◽  
Seminiferous Epithelium ◽  
Lower Serum ◽  
Infertile Men ◽  
Serum Lh ◽  
Leydig Cell Function

Abstract To investigate whether an impaired Leydig cell function is present in severely oligospermic men, serum testosterone (T), LH, estradiol (E2), and SHBG levels in 357 idiopathic infertile men were compared with levels in 318 proven fertile men. In addition, the T/LH ratio, E2/T ratio, and calculated free T index (cFT) were compared between the two groups. A shift toward lower serum T levels, cFT, and T/LH ratio and higher serum LH, E2, and E2/T levels was observed in the group of infertile men. On average, the infertile men had 18, 26, and 34% lower serum T, cFT, and T/LH levels, respectively, and 19, 18, and 33% higher serum LH, E2, and E2/T levels, respectively, than the fertile men. Twelve percent of the infertile men had a serum T level that fell below the 2.5 percentile of the fertile levels, and 15% of the infertile men had a LH level that was above the 97.5 percentile of the fertile levels. Thus, the group of infertile men showed significant signs of impaired Leydig cell function in parallel to their impaired spermatogenesis. The association of decreased spermatogenesis and impaired Leydig cell function might reflect a disturbed paracrine communication between the seminiferous epithelium and the Leydig cells, triggered by distorted function of the seminiferous epithelium. On the other hand, the parallel impairment of spermatogenesis and Leydig cells may reflect a congenital dysfunction of both compartments caused by a testicular dysgenesis during fetal/infant development.

scholarly journals Decrease in semen quality and Leydig cell function in infertile men: a longitudinal study

2018 ◽  
Vol 33 (11) ◽  
pp. 1963-1974 ◽  
Author(s):  
I A Olesen ◽  
U N Joensen ◽  
J H Petersen ◽  
K Almstrup ◽  
E Rajpert-De Meyts ◽  
...  
Keyword(s):  
Longitudinal Study ◽  
Leydig Cell ◽  
Cell Function ◽  
Semen Quality ◽  
Infertile Men ◽  
Leydig Cell Function

INSL3: A Marker of Leydig Cell Function and Testis-Bone-Skeletal Muscle Network

2020 ◽  
Vol 27 (12) ◽  
pp. 1246-1252
Author(s):  
Paolo Facondo ◽  
Andrea Delbarba ◽  
Filippo Maffezzoni ◽  
Carlo Cappelli ◽  
Alberto Ferlin
Keyword(s):  
Skeletal Muscle ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Cell Damage ◽  
Endocrine Function ◽  
Testicular Descent ◽  
Male Hypogonadism ◽  
Adult Men ◽  
Leydig Cell Function

This article reviews the role of INSL3 as biomarker of Leydig cell function and its systemic action in testis-bone-skeletal muscle crosstalk in adult men. Insulin-like factor 3 (INSL3) is a peptide hormone secreted constitutively in a differentiation-dependent mode by testicular Leydig cells. Besides the role for the testicular descent, this hormone has endocrine anabolic functions on the bone-skeletal muscle unit. INSL3 levels are low in many conditions of undifferentiated or altered Leydig cell status, however the potential clinical utility of INSL3 measurement is not yet well defined. INSL3 levels are modulated by the long-term cytotropic effect of the hypothalamicpituitary- gonadal axis, unlike testosterone that is acutely sensitive to the stimulus by luteinizing hormone (LH). INSL3 directly depends on the number and differentiation state of Leydig cells and therefore it represents the ideal marker of Leydig cell function. This hormone is more sensitive than testosterone to Leydig cell impairment, and the reduction of INSL3 in adult men can precociously detect an endocrine testicular dysfunction. Low INSL3 levels could cause or contribute to some symptoms and signs of male hypogonadism, above all sarcopenia and osteoporosis. The measurement provided suggested that the measurement of INSL3 levels should be considered in the clinical management of male hypogonadism and in the evaluation of testicular endocrine function. The monitoring of INSL3 levels could allow an early detection of Leydig cell damage, even when testosterone levels are still in the normal range.

scholarly journals Autoradiographical Localization of Luteinizing Hormone Releasing Hormone (LHRH) Receptors on Rat Testicular Intertubular Cells Fractionated on Percoll Density Gradients

1985 ◽  
Vol 38 (4) ◽  
pp. 435 ◽  
Author(s):  
MP Hedger ◽  
OP Risbridger ◽  
DM de Kretser
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Specific Binding ◽  
Density Gradients ◽  
Direct Stimulation ◽  
Density Region ◽  
Luteinizing Hormone Releasing Hormone ◽  
Testicular Cells ◽  
Leydig Cell Function

The specific binding of 125I-1abelled [D-Ser(tBu)6,des-GlyNH21OJ LHRH ethylamide (LHRH-A) to testicular intertubular cells fractionated on Percoll density gradients was investigated. The greatest binding per cell occurred in the density region which contained the largest proportion of Leydig cells (sp. gr. 1�0820-1�0585). Autoradiographs of the cells from this region confirmed that silver stains were predominantly located over the Leydig cell, significantly (P < 0�01) more grains were observed over this cell type in the total binding fractions than in the non-specific binding fractions. However, 5�9% of cells other than Leydig cells (testicular macrophages and indeterminate connective tissue cells) from this region also displayed significant disp1aceable binding (P < 0�01). The location of HRH-A binding to cells in other density regions, which did not contain identifiable Leydig cells, could not be established by autoradiography. These results confirm that the Leydig cell possesses LHRH receptors, but also indicate that other testicular cells have specific, highaffinity binding sites for LHRH-A, and may either be responsive to direct stimulation by LHRH, or may partially mediate the effects of LHRH and its agonists on Leydig cell function.

Bisphenol A decreases expression of insulin-like factor 3 and induces histopathological changes in testes of rat

2021 ◽  
pp. 074823372110140
Author(s):  
Leman Sencar ◽  
Gulfidan coskun ◽  
Dilek Şaker ◽  
Tuğçe Sapmaz ◽  
Abdullah Tuli ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Leydig Cell ◽  
Cell Function ◽  
Light And Electron Microscopy ◽  
Serum Testosterone ◽  
Testicular Atrophy ◽  
Male Rats ◽  
Chemical Agent ◽  
High Doses ◽  
Leydig Cell Function

Bisphenol A (BPA) is a chemical agent known to have detrimental reproductive and developmental effects. The tissue-specific impacts of BPA exposures and target tissues sensitiveness to BPA are still unclear. The aim of this study was to determine the short- and long-term dose-dependent toxic effects of BPA on rat testes. Forty-eight Wistar albino male rats were divided into four groups each containing 12 rats. To induce toxicity, BPA was administered orally at three different dosages (50, 100, and 200 mg/kg) for 14 and 28 days, respectively. Testis tissues were examined using light and electron microscopy, immunohistochemistry, and biochemical methods. Serum testosterone (T) and luteinizing hormone (LH) levels were measured. Additionally, insulin-like factor 3 (INSL3) as a marker of Leydig cell function was evaluated immunohistochemically. Groups administered high doses of BPA showed severe degenerations such as testicular atrophy, spermatogenic arrest, and interstitial edema in testis. Also, a significant decrease in INSL3 immunoreactivity and serum LH and T levels was found. The results indicated that both increased exposure time and dosage of BPA caused more serious detrimental effects on testes in the rat. Decreased INSL3 and T levels was evidence of Leydig cell function impairment due to BPA.

Effects of recombinant human FSH in immature hypophysectomized male rats: evidence for Leydig cell-mediated action on spermatogenesis

1994 ◽  
Vol 141 (3) ◽  
pp. 449-457 ◽  
Author(s):  
T Matikainen ◽  
J Toppari ◽  
K K Vihko ◽  
I Huhtaniemi
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Serum Testosterone ◽  
Male Rats ◽  
Seminiferous Tubules ◽  
Spermatogenic Cells ◽  
Hypophysectomized Rats ◽  
First Time ◽  
Recombinant Human Fsh

Abstract The mode of FSH actions within the testis was studied in immature hypophysectomized male rats by treatment with recombinant human FSH (recFSH, Org 32489). To elucidate the involvement of Leydig cells and androgens in the maintenance of spermatogenesis in FSH-treated hypophysectomized rats further, the recFSH treatment was given both alone and after destruction of Leydig cells with ethane-1,2-dimethane sulphonate (EDS). Three days after hypophysectomy (at 31 days of age) the rats were given one i.p. injection of vehicle or EDS and, 4 days later, they were implanted with osmotic minipumps releasing either 0·9% (w/v) NaCl or 1 IU recFSH/day. Recombinant FSH alone increased testicular weights 2·5-fold in 7 days (P<0·01). The effect of FSH was similar in EDS-pretreated rats (P<0·01). Testicular testosterone increased from 6·5 ± 1·6 to 16·9 ± 5·3 (s.e.m.) pmol/g tissue (P<0·05) and serum testosterone from 0·12 ± 0·02 to 0·22 ± 0·03 nmol/l (P<0·05) when the rats were treated with recFSH. EDS alone did not affect testicular testosterone but, when combined with recFSH, it totally abolished the stimulatory effect of FSH on testosterone. Testicular binding of 125I-labelled iodo human chorionic gonadotrophin (hCG) and 125I-labelled iodo recFSH was increased 2·5- and 2·1-fold respectively with recFSH treatment (P<0·01). EDS, either alone or with FSH, abolished specific testicular hCG binding (P<0·01), but had no effect on that of recFSH. However, FSH increased its own receptors only in animals not treated with EDS. Histological analysis of the testes revealed that the diameters of the seminiferous tubules increased from 115 ± 6·1 to 160 ± 7·2 μm (P<0·05) with recFSH, and a comparable increase was observed when EDS treatment preceded that of recFSH (143 ± 1·5 μm, P<0·05 vs. controls). Quantification of the spermatogenic cells indicated that recFSH supported the progression of spermatogenesis, as shown by increased number of meiotic and haploid spermatogenic cells (P<0·05). In all EDS-treated animals, spermatogenesis was severely disturbed and only a few spermatids were seen. In conclusion: (1) these results further support the suggestion that FSH has indirect stimulatory effects on Leydig cell function, (2) the completion of meiosis and spermiogenesis are supported by FSH, the effect of which is enhanced by the presence of Leydig cells, suggesting its dependence on androgens, and (3) we show for the first time that FSH is able to stimulate its own receptors only in the presence of Leydig cell-derived factors, probably androgens. Journal of Endocrinology (1994) 141, 449–457

Expression of the glucocorticoid receptor and 11β-hydroxysteroid dehydrogenase 2 in pig testes cells along fetal development

2007 ◽  
Vol 19 (5) ◽  
pp. 664 ◽  
Author(s):  
S. Haeussler ◽  
R. Claus
Keyword(s):  
Germ Cells ◽  
Leydig Cell ◽  
Fetal Development ◽  
Leydig Cells ◽  
Cell Function ◽  
Hydroxysteroid Dehydrogenase ◽  
Immunocytochemical Staining ◽  
Tunel Staining ◽  
Steroid Synthesis ◽  
Leydig Cell Function

The glucocorticoid (GC)–cortisol receptor (GCR)–11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) system is involved in the regulation of Leydig cell function and spermatogenesis in mature animals. Herein, we describe the expression of the GCR and 11β-HSD2 and the occurrence of apoptosis during fetal development. Male fetuses were collected from Weeks 6, 10, 13, and 15 of pregnancy and from neonates. The testes were used for the immunocytochemical staining of GCR, 11β-HSD2 and for terminal deoxyribonucleotidyl transferase-mediated dUTP–digoxigenin nick end-labelling (TUNEL) staining of apoptosis. Apoptosis did not occur in any Leydig cells, but approximately 30% expressed GCR and 11β-HSD2. The number of GCR-positive cells was similar at all stages, but the number of 11β-HSD2-positive cells tended to be higher at Weeks 6 and 15. Steroid synthesis was also higher compared with Weeks 10 and 13. Apoptosis occurred in only a few germ cells. Nearly all germ cells were GCR positive at Weeks 10 and 13, when 11β-HSD2 was also increased. The total number of 11β-HSD2-positive germ cells was approximately 30%. Thus, elevated GCR expression coincided with the differentiation of gonocytes to spermatogonia and their migration to the basal lamina.

CHANGES IN LEYDIG CELL HYDROXYSTEROID DEHYDROGENASES INDUCED BY ADMINISTRATION OF TESTOSTERONE PROPIONATE TO NORMAL MEN

1974 ◽  
Vol 60 (1) ◽  
pp. 175-NP ◽  
Author(s):  
H. C. MORSE ◽  
C. G. HELLER
Keyword(s):  
Leydig Cell ◽  
Leydig Cells ◽  
Cell Function ◽  
Testosterone Propionate ◽  
Testicular Biopsy ◽  
Frozen Sections ◽  
Histochemical Technique ◽  
Biopsy Specimens ◽  
Normal Men ◽  
Leydig Cell Function

SUMMARY By the employment of an improved histochemical technique, frozen sections from human testicular biopsy specimens were examined for 3β-and 17β-hydroxysteroid dehydrogenase (HSD) activity, before, during, and after administration of 25 or 50 mg testosterone propionate per day to normal men. This administration strongly suppressed Leydig cell HSD activity and caused these cells to be transformed into fibroblast-like cells. After cessation of administration, the Leydig cells recovered morphologically and so did, simultaneously their 3β- and 17β-HSD activity. It is concluded that histochemically detectable 3β- and 17β-HSD are under gonadotrophin control and change with alterations in Leydig cell function. The morphology or 3β- and 17β-HSD are therefore probably acceptable as indicators of Leydig cell function in reproductively normal men.

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