AbstractMammalian sperm are stored in the epididymis in a dormant state. Upon ejaculation, they must immediately start producing sufficient energy to maintain motility and support capacitation. While this increased energy demand during capacitation is well-established, it remains unclear how mouse sperm modify their metabolism to meet this need. We now show that capacitating mouse sperm enhance glucose uptake, identifying glucose uptake as a functional marker of capacitation. Using an extracellular flux analyzer, we show that glycolysis and oxidative phosphorylation increase during capacitation. Furthermore, this increase in oxidative phosphorylation is dependent on glycolysis, providing experimental evidence for a link between glycolysis and oxidative phosphorylation in mouse sperm.
Mammalian sperm acquire fertilization capacity in the female reproductive tract in a process known as capacitation. During capacitation, sperm change their motility pattern (i.e., hyperactivation) and become competent to undergo the acrosome reaction. We have recently shown that, in the mouse, sperm capacitation is associated with increased uptake of fluorescently labeled deoxyglucose and with extracellular acidification suggesting enhanced glycolysis. Consistently, in the present work we showed that glucose consumption is enhanced in media that support mouse sperm capacitation suggesting upregulation of glucose metabolic pathways. The increase in glucose consumption was modulated by bicarbonate and blocked by protein kinase A and soluble adenylyl cyclase inhibitors. Moreover, permeable cyclic adenosine monophosphate (cAMP) agonists increase glucose consumption in sperm incubated in conditions that do not support capacitation. Also, the increase in glucose consumption was reduced when sperm were incubated in low calcium conditions. Interestingly, this reduction was not overcome with cAMP agonists. Despite these findings, glucose consumption of sperm from Catsper1 knockout mice was similar to the one from wild type suggesting that other sources of calcium are also relevant. Altogether, these results suggest that cAMP and calcium pathways are involved in the regulation of glycolytic energy pathways during murine sperm capacitation.
Capítulo 2/Chapter 2: Introducción y planteamiento ………………………………….. 31 Capítulo 3/Chapter 3: Revisión bibliográfica …………………………………………. 42 Capítulo 4/Chapter 4: Objetivos/Objectives …………………………………………... 97 Capítulo 5/Chapter 5: Influence of gonadotrophin-induced first estrus on gilt fertility. 103 Capítulo 6/Chapter 6: Influence of lactation length and gonadotrophins administered at weaning on fertility of primiparous sows ……………………………………………….. 122 Capítulo 7/Chapter 7: Relationship between estrus responses of prepubertal gilts to gonadotrophin treatment and subsequent sow fertility and retention to parity four ……. 139 Capítulo 8/Chapter 8: Relationship between vaginal mucus conductivity and time of ovulation in weaned sows ………………………………………………………………. 154 Capítulo 9/Chapter 9: Resumen global de metodología y resultados ………………… 173 Capítulo 10/Chapter 10: Discusión general …………………………………………... 187 Capítulo 11/Chapter 11: Conclusiones/Conclusions …………………………………. 203 Capítulo 12/Chapter 12: Bibliografía ………………………………………………… 212 Examination of fertility in estrus-induced gilts Influence of gonadotrophin-induced first estrus on gilt fertility; D.
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