Relationship between semen parameters, serum InhB, and INSL-3 levels, and the degree of varicocele

Abstract Background Varicocele is an abnormal expansion of the pampininias venous plexus in the scrotum, resulting in impaired sperm production and reduced sperm quality. The exact pathophysiological mechanism leading to varicocele-related infertility has not been fully elucidated. Although treatable, varicocele may lead to male infertility. Objective To investigate the relationship between semen parameters, serum InhB and INSL-3 levels, and the degree of varicocele in male patients. Methods Serum InhB and INSL-3 were detected. To evaluate the relationship between semen parameters and serum InhB and INSL-3 levels. To evaluate the value of semen parameters and serum InhB and INSL-3 levels in distinguishing disease severity in patients with varicocele. Results Serum INSL-3 in patients with varicocele decreased with the severity of the disease. Serum INSL-3 was positively correlated with total sperm count and frequency of normal sperm morphology. There was a weak correlation between serum InhB and semen volume, concentration, and total sperm. Patients with different disease severity were similar within the groups, with partial overlap or similarity between varicocele Grade I and Grade II, and significant differences between Grade III and Grade I and II. Semen volume, concentration, total sperm, normal sperm morphology, and serum InhB and INSL-3 levels could distinguish the degree of varicocele. Conclusion Semen parameters and the combination of serum InhB and INSL-3 levels in patients with varicocele are closely related to the severity of the disease. Serum INSL-3 is expected to be a potential biomarker for early clinical intervention.

Leydig and Sertoli cell function in individuals with genital ambiguity, 46,XY karyotype, palpable gonads and normal testosterone secretion: a case-control study

Abstract BACKGROUND: Because normal male sexual differentiation is more complex than normal female sexual differentiation, there are more cases of disorders of sex development (DSDs) with 46,XY karyotype that have unclear etiology. However, Leydig and Sertoli cell markers are rarely used in distinguishing such individuals. OBJECTIVES: To evaluate the function of Leydig and Sertoli cells in individuals with genital ambiguity, 46,XY karyotype, palpable gonads and normal testosterone secretion. STUDY DESIGN AND SETTING: Case-control study with 77 patients, including eight with partial androgen insensitivity syndrome, eight with 5α-reductase deficiency type 2 (5ARD2) and 19 with idiopathic 46,XY DSD, and 42 healthy controls, from the Interdisciplinary Study Group for Sex Determination and Differentiation (GIEDDS), at the State University of Campinas (UNICAMP), Campinas, Brazil. METHODS: Baseline levels of gonadotropins, anti-Müllerian hormone (AMH), inhibin B, insulin-like 3 (INSL3), testosterone and dihydrotestosterone in cases, and AMH, inhibin B, and INSL3 levels in controls, were assessed. RESULTS: There was no significant difference in age between cases and controls (P = 0.595). AMH and inhibin B levels were significantly lower in cases than in controls (P = 0.031 and P < 0.001, respectively). INSL3 levels were significantly higher in cases than in controls (P = 0.003). Inhibin B levels were lower in 5ARD2 patients (P = 0.045) and idiopathic patients (P = 0.001), in separate comparisons with the controls. CONCLUSION: According to our findings, we can speculate that inhibin B levels may be used to differentiate among DSD cases.

Insulin 3-like hormone and its role in epididymo-testicular descent

PURPOSE: The role of insulin 3-like (Insl3) hormone signaling in the testicular descent process has been demonstrated. The purpose of the present study was to evaluate epididymal development in Insl3-deficient mice. MATERIALS AND METHODS: Heterozygous and homozygous Insl3 mutants of a mixed CD1 X 129/Sv genetic background were generated by breeding Insl3-/- females with Insl3+/- males, and their genotypes were determined by polymerase chain reaction. On the first postnatal day, newborn males were sacrificed, embedded in paraffin, and cut in 4 µm sections. Sections were stained with hematoxylin/eosin and immunoreacted with anti-± actin antibody. RESULTS: An analysis of stained sections indicated an arrest in the development of the epididymis in all homozygous mice. The cauda and corpus of the epididymis were undersized. Compared to the heterozygous epididymis, the homozygous epididymis had fewer peritubular layers and dwarfish musculature. We confirmed this with immunostaining with monoclonal antibodies against ± -smooth muscle actin. CONCLUSION: Defective development of the smooth musculature in the epididymis of Insl3 homozygous mutant mice, combined with its high intraabdominal undescended position, supports previous observations regarding the importance of intact epididymis morphology and function for descent of the epididymo-testicular unit.

The change of the mRNA expression of INSL3 gene in perinatal mice leydig cells exposed to diethylstilbestrol in vivo and in vitro / 重庆医科大学学报

Objective:To explore the mRNA expression of INSL3 gene in perinatal mice Leydig cells exposed to diethylstilbestrol(DES) in vivo and in vitro.Methods:The Leydig cells were isolated from fetal mouse testis and were cultured in DMEM/F12 medium and identified by 3 beta-hydroxysteroid dehydrogenase(3?-HSD).Reverse transcriptase-polymerase chain reaction(RT-PCR)and in situ hybridization were used for examination of the expression levels of INSL3 mRNA in primarily cultured Leydig cells incubated with DES(at the dose of 1?g/L,5?g/L and 25?g/L,respectively).Pregnant mice were exposed to DES at the dose of 1,10 or 100?g/kg body weight per day by gavage from gestation day(GD)12 to postnatal day(PND)3.The expression of INSL3 gene in neonatal mouse testis was investigated by RT-PCR.Results:Histological alterations of primarily cultured Leydig cells and neonatal mouse testis exposed to DES were observed.The expression level of INSL3 mRNA in DES treated groups including the primarily cultured Leydig cells and male mouse offspring’s testis were lower than those of the control groups.Conclusion:DES can downregulate the expression level of INSL3 mRNA in Leydig cells in vitro and in vivo.It may be a possible mechanism that DES interferes with gubernaculum development and cause cryptorchidism.