Furthermore, NADH is directly implicated in sperm capacitation, the maturation process required for oocyte fertilization. In rodent testes, visfatin stimulates steroidogenesis and promotes Leydig cell proliferation, thereby reinforcing local androgen synthesis.
Conversely, pathological expansion of VAT leads to local resistance against the protective actions of these adipokines, culminating in a systemic disruption of steroidogenesis and cavernous vasodynamics,
The NAD⁺ and reduced NADH generated through visfatin's enzymatic activity regulate Sertoli cell function and sustain mitochondrial oxidative phosphorylation, which is essential for sperm motility.
Within the male genital tract, visfatin fulfills a pivotal bioenergetic role. It is present in human seminal plasma at concentrations approximately 100-fold higher than in serum, pointing to a specialized local function.
It exhibits dual functionality: extracellularly, it operates as a pleiotropic hormone, whereas intracellularly, it catalyzes the rate-limiting step in the synthesis of nicotinamide adenine dinucleotide (NAD⁺), a coenzyme essential for cellular energy metabolism.
Visfatin: Enzymatic Role in Sperm Function and the Gonadotropic Axis
Visfatin, also known as nicotinamide phosphoribosyltransferase (NAMPT), is a 56 kDa adipokine produced in significant quantities by visceral adipose tissue and immune cells.
This mechanism shields the male reproductive tract from excessive estrogenic feedback, thereby maintaining steady testosterone production and safeguarding libido and spermatogenesis.