The Fate of Leydig Cells in Men with Spermatogenic Failure.

The steroidogenic cells in the testicle, Leydig cells, located in the interstitial compartment, play a vital role in male reproductive tract development, maintenance of proper spermatogenesis, and overall male reproductive function. Therefore, their dysfunction can lead to all sorts of testicular pathologies. Spermatogenesis failure, manifested as azoospermia, is often associated with defective Leydig cell activity. Spermatogenic failure is the most severe form of male infertility, caused by disorders of the testicular parenchyma or testicular hormone imbalance. This review covers current progress in knowledge on Leydig cells origin, structure, and function, and focuses on recent advances in understanding how Leydig cells contribute to the impairment of spermatogenesis.

The Association between Vitamin D and the Components of Male Fertility: A Systematic Review.

OBJECTIVE: Previous systematic reviews of the effects of vitamin D on the components of male fertility have been inconclusive. This article systematically reviews the latest research to examine the relationship between vitamin D, semen quality parameters, and sex hormones production. METHODS: MEDLINE, Cochrane, and Web of Science databases were searched using the appropriate keywords. RESULTS: Observational studies indicate significant correlation between vitamin D levels and sperm parameters, with a particular emphasis on sperm motility, and partially suggest a relationship between higher serum testosterone and vitamin D levels. Additionally, interventional studies confirmed that vitamin D supplementation has a positive effect on sperm motility, especially progressive. However, most randomized clinical trials indicate that vitamin D treatment does not have any significant effect on testosterone or other hormone levels. CONCLUSIONS: Although our findings add to the discussion regarding the effect of vitamin D on male fertility, there is still no solid evidence to support the use of vitamin D supplementation to improve the outcomes of patients with impaired sperm parameters and hormonal disorders. Additional dedicated clinical studies are needed to clarify the relationship between vitamin D and male fertility, along with its components.

Features of gonadal dysgenesis and Leydig cell impairment in testes with Sertoli cell-only syndrome.

INTRODUCTION: There is evidence that disturbed spermatogenesis is associated with impaired Leydig cell function and that it may be the result of testicular dysgenesis during fetal/infant development. Sertoli cell-only syndrome (SCOS) is defined by complete lack of germ cells in the seminiferous epithelium. The pathogenesis of SCOS is still not well understood. The aim of the study is to evaluate testes with SCOS focusing on morphometric signs of testicular dysgenesis and markers of Leydig cell (LC) function in relation to hormonal status of studied infertile men. MATERIALS AND METHODS: Forty-nine testicular biopsies of patients with SCOS and 15 controls with normal spermatogenesis (NOR) were studied. In each biopsy the seminiferous tubule diameter (STD), thickness of tubular membrane (TM), area fraction of intertubular space (AFIS) were measured and semi-quantitative assessment of the LC number was performed (LC-score). The results of histological examination were correlated with serum levels of FSH, LH, testosterone (T) and T/LH ratio. RESULTS: In SCOS group testicular volume (median [M]: 16.0 vs. 29.5; p < 0.001) and STD (M: 141.7 vs. 190.2; p < 0.001) were lower, while TM (M: 9.8 vs. 6.4; p < 0.001) and AFIS (M: 47.6 vs. 27.6; p < 0.001) were significantly higher in comparison to NOR group. LC-score was higher in SCOS than in NOR group (M: 2.2 vs. 1.1; p < 0.001). Abnormal AFIS and STD were present in 43% of SCOS biopsies and among them in 81% the increased LC-score was found. In SCOS group, the subjects had significantly higher levels of both gonadotropins (FSH, M: 19.9 vs. 3.4; p < 0.001; LH, M: 7.1 vs. 4.2; p < 0.001). Total serum testosterone level did not differ between studied groups; however, T/LH ratio was significantly lower in SCOS group (M: 2.3 vs. 3.8; p < 0.001). Negative correlation between LC-score and STD was observed in SCOS group (r = -0.48; p < 0.001). AFIS correlated positively with serum FSH level in NOR (r = 0.53; p < 0.05) and SCOS (r = 0.41; p < 0.05) group, while with LH, and negatively with T/LH ratio, only in SCOS (LH, r = 0.37; p < 0.05; T/LH, r = -0.36; p < 0.05) group. CONCLUSIONS: We have shown that substantial number of testes from subjects with SCOS presented abnormal morphometric features, which are recognized as the signs of testicular dysgenesis. Additionally, an increased number of Leydig cells simultaneously with abnormal T/LH ratio were found, which suggests an impaired function of these cells. Increased serum levels of LH and also FSH, may reflect dysfunction of Leydig cells. It seems that reproductive hormones levels reflect also the condition of testicular structure, and that FSH may be related to the changes in intertubular space area independently of impaired Leydig cell function.