Sperm motility

About: Sperm motility is a research topic. Over the lifetime, 13874 publications have been published within this topic receiving 416587 citations. The topic is also known as: sperm movement & GO:0097722.

Vitamin D and male reproduction

Abstract: Vitamin D is a versatile signalling molecule with a well-established role in the regulation of calcium homeostasis and bone health. The spectrum of vitamin D target organs has expanded and the reproductive role of vitamin D is highlighted by expression of the vitamin D receptor (VDR) and enzymes that metabolize vitamin D in testis, male reproductive tract and human spermatozoa. The expression levels of VDR and CYP24A1 in human spermatozoa serve as positive predictive markers of semen quality, and VDR mediates a nongenomic increase in intracellular calcium concentration that induces sperm motility. Interestingly, functional animal models show that vitamin D is important for estrogen signalling and sperm motility, while cross-sectional studies support the positive association between serum 25-hydroxyvitamin D level and sperm motility in both fertile and infertile men. Expression of VDR and enzymes that metabolize vitamin D in fetal testis indicates a yet unknown role during development, which may be extrapolated from invasive testicular germ cell tumours where 1α,25-dihydroxyvitamin D induces a mesodermal differentiation of the pluripotent testicular cancer cells. Taken together, vitamin D signalling has a positive effect on semen quality, increases estrogen responsiveness and differentiates germ cell tumours. Future studies are needed to determine when 1α,25-dihydroxyvitamin D acts in a paracrine manner and whether systemic changes, which are subject to pharmacological modulation, could influence male reproductive function.

Mice deficient in the axonemal protein Tektin-t exhibit male infertility and immotile-cilium syndrome due to impaired inner arm dynein function.

Abstract: The haploid germ cell-specific Tektin-t protein is a member of the Tektin family of proteins that form filaments in flagellar, ciliary, and axonemal microtubules. To investigate the physiological role of Tektin-t, we generated mice with a mutation in the tektin-t gene. The homozygous mutant males were infertile, while the females were fully fertile. Sperm morphology and function were abnormal, with frequent bending of the sperm flagella and marked defects in motility. In vitro fertilization assays showed that the defective spermatozoa were able to fertilize eggs. Electron microscopic examination showed that the dynein inner arm structure was disrupted in the sperm flagella of tektin-t-deficient mice. Furthermore, homozygous mutant mice had functionally defective tracheal cilia, as evidenced by altered dynein arm morphology. These results indicate that Tektin-t participates in dynein inner arm formation or attachment and that the loss of Tektin-t results in impaired motility of both flagella and cilia. Therefore, the tektin-t gene is one of the causal genes for immotile-cilium syndrome/primary ciliary dyskinesia.

Energy metabolism and sperm function

Abstract: Energy metabolism is a key factor supporting sperm function. Sustaining sperm motility and active protein modifications such as phosphorylation could be the reason why sperm require exceptionally more ATP than other cells. Many methods have been used to understand the relationship between energy metabolism and sperm function. These approaches have identified critical metabolic pathways that support specific processes during germ cell development and fertilisation. In round spermatids, lactate and pyruvate are the preferred substrates and the use of glucose is limited, however, during epididymal maturation sperm expand to use glycolysis. While the acrosome reaction requires lactate or pyruvate for ATP production by oxidative phosphorylation, gamete fusion requires glucose to produce NADPH by the pentose phosphate pathway. Sperm motility appears to be supported by relatively low ATP levels, but achievement of high ATP levels are essential for tyrosine phosphorylation linked to hyperactivation. Thus, each individual process and event requires a different substrate and metabolic pathway. Despite different preferences for energy substrates and metabolic pathways between species, analysis of knockout mice revealed that glycolysis is indispensable for mouse sperm function and that oxidative phosphorylation is not essential for male fertility. This suggests that glycolysis could compensate for the lack of oxidative phosphorylation and recover most sperm function. Spermatogenic cell-specific glycolytic enzymes may confer flexible use of substrates and adapt to unexpected conditions for substrates in the female reproductive tract.