Core function: The "switch" of the reproductive axis

1. The key trigger for the onset of puberty

Before puberty, the Kisspeptin-GPR54 system is inhibited (possibly related to endogenous opioid peptides or gamma-aminobutyric acid); when entering puberty, the inhibition is lifted, a large amount of Kisspeptin-10 is released, stimulating the secretion of GnRH and initiating sexual development (such as ovarian/testicular maturation and the appearance of secondary sexual characteristics).

2. Homeostatic Regulation of Adult Reproductive Function

Female:

During the menstrual cycle, the estrogen peak at ovulation enhances the stimulation of Kisspeptin - 10 on GnRH through positive feedback, triggering the LH surge and ovulation.

Maintain the function of the corpus luteum and regulate the endometrial receptivity.

Male:

Promote the pituitary gland to secrete LH, stimulate the Leydig cells of the testis to synthesize testosterone, and regulate spermatogenesis.

3. Cross-regulation of Energy Metabolism and Reproduction

Obesity or malnutrition can affect the activity of Kiss1 neurons through metabolic signals such as leptin:

Lack of leptin (such as congenital leptin deficiency) inhibits Kisspeptin secretion, leading to delayed puberty and hypogonadism.

Chronic hyperglycemia may interfere with the Kisspeptin-GPR54 pathway through inflammatory factors, explaining the association between metabolic diseases and infertility.

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