Capacitation increases glucose consumption in murine sperm.

Area of Science:

• Reproductive Biology
• Sperm Physiology
• Cellular Metabolism

Background:

• Mammalian sperm capacitation is essential for fertilization, involving motility changes and acrosome reaction competence.
• Previous work indicated increased glucose uptake and glycolysis during mouse sperm capacitation.

Purpose of the Study:

• To investigate the regulation of glucose metabolism during mouse sperm capacitation.
• To elucidate the roles of cyclic adenosine monophosphate (cAMP) and calcium in this process.

Main Methods:

• Measurement of glucose consumption in mouse sperm under various conditions.
• Inhibition studies using protein kinase A and soluble adenylyl cyclase inhibitors.
• Experiments with cAMP agonists and varying calcium concentrations, including in Catsper1 knockout mice.

Main Results:

• Enhanced glucose consumption was observed in media supporting sperm capacitation, indicating upregulated glycolysis.
• Bicarbonate modulated glucose consumption, while PKA and sAC inhibitors blocked it.
• cAMP agonists increased glucose consumption, and low calcium reduced it, an effect not overcome by cAMP.
• Catsper1 knockout sperm showed similar glucose consumption to wild-type, suggesting alternative calcium sources.

Conclusions:

• Cyclic adenosine monophosphate (cAMP) and calcium signaling pathways are key regulators of glycolytic energy pathways during murine sperm capacitation.
• These findings highlight the metabolic reprogramming necessary for sperm to gain fertilization capacity.