Fertilisation Promoting Peptide: a key player in male fertility/subfertility?

Abstract

‘Male factor’ problems contribute to subfertility in a significant proportion of couples. In some instances, defective sperm production has qualitative and/or quantitative effects on the semen profile; in others, no obvious defects can be detected, yet spermatozoa are non-fertilising. Recent studies have revealed that fertilisation promoting peptide (FPP), which is structurally related to thyrotrophin releasing hormone (TRH) and found in the prostate gland and seminal plasma of many mammals, has important biologically relevant effects on both mouse and human spermatozoa. In the presence of physiological concentrations of FPP, spermatozoa become fertile more quickly and are then inhibited from undergoing spontaneous acrosome loss, a step that would render them non-fertilising. In vivo, these responses could be extremely important in maximising fertilising potential of the few spermatozoa that reach the site of fertilisation. Prostatic dysfunction results in decreased production of FPP and increased production of less bioactive FPP-related peptides. A putative receptor (TCP-11) for FPP has been identified in the mouse; the gene (with a human homologue) which codes for TCP-11 resides within a complex known to contain genes affecting male fertility. These results strongly suggest that FPP plays an important role in normal fertility and that it might therefore provide both new therapeutic approaches for some cases of unexplained infertility and new approaches for male contraception.