Follicle-Stimulating Hormone Receptor Polymorphism in Infertile Palestinian Men

Abstract

Background: Follicle stimulating hormone (FSH) is a pituitary glycoprotein, which is necessary for normal reproduction in both male and female mammals. Follicle stimulating hormone receptor (FSHR) signaling stimulates proliferation of Sertoli cells and maintains normal sperm production (spermatogenesis). The 2 most common single-nucleotide polymorphisms (SNPs) are Thr307Ala and Asn680Ser polymorphisms in the FSHR gene that have possible associations with the male infertility. Objective: This study aimed to investigate FSHR polymorphism in infertile Palestinian men. Materials and Methods: This study is case-control study comprised 56 Palestinian males grouped into 24 normozoospermic healthy controls (normal sperm count≥20 X 106/ml), and 32 infertile males. Infertile males were grouped into 11 azoospermic males (zero sperm count), and 21 oligozoospermic males (sperm count <15 X 106/ml). Semen analysis, Follicle stimulating hormone (FSH), Luteinizing hormone (LH) and Total testosterone were determined used ELISA proceure. Blood samples were collected from patients for DNA extraction. Allelic variant of FSHR gene was determined by PCR-RFLP technique. Data were analyzed using SPSS version 21. Results: The mean sperm count of azoospermic, oligospermic and normal men were found to be 0.0±0.0, 5.7±4.4 and 39.8±11.7 X 106/ml. Sperm count revealed significant differences between control and oligospermia, and between control and azoospermia (P=0.000, 95% CI 27.9 to 40.3 and P=0.000, 95% CI 32.3 to 47.3, respectively). In addition, sperm count was significantly decreased in oligospermia compared to control (P= 0.000, 95% CI -40.3 to -27.9). Sperm motility in terms of activity, sluggish and dead sperms showed significant differences between the different groups of men (activity: F=195.32, P=0.000; sluggish: F=123.93, P=0.000 and dead: F=326.02, P=0.000). LH and FSH were significantly increased in azoospermia compared to controls (P=0.000, 95% CI 6.3 to 1.9 and P=0.000, 95% CI 24.7 to 12.3, respectively) and compared to oligospermia (P=0.003, 95% CI 5.4 to 0.9 and P=0.000, 95% CI 20.1 to 7.4 respectively). The mean level of T testosterone was significantly decreased in oligospermia and azoospermia compared to controls (P=0.000, 95% CI -1.4 to -3.3 and P=0.000, 95% CI -2.2 to -4.4 respectively). The SNPs of FSHR allele frequency distributed among the three groups was about 33.93%. That showed no significant difference in the prevalence of FSHR among the three groups (X2=8.428, P=0.077). Sperm count was significantly decreased in mutant (Ser/Ser) FSHR allele compared to wild (Asn/Asn) FSHR allele (2.5±2.8 versus 24.6±19.8, P=0.044). On the other hand, active, sluggish and dead sperm parameters showed no significant differences among various groups (P>0.05). LH was significantly increased in mutant (Ser/Ser) FSHR allele compared to wild (Asn/Asn) FSHR allele (8.1±3.4 versus 4.7±1.6, P=0.025), whereas the T testosterone was significantly decreased in mutant (Ser/Ser) FSHR allele compared to wild (Asn/Asn) FSHR allele (2.8±1.1 versus 4.9±1.7, P= 0.041). However, there was no significant difference in FSH levels among various groups (P>0.05). Conclusions: We conclude that the presence of mutant (Ser/Ser) FSHR allele is observed to be a cause for a decreased in a sperm count and T testosterone and increased of LH level.