This is manifested as increased hypothalamic GnRH secretion, initial decreases followed by increases in FSH and LH levels, delayed changes in serum estradiol (E2) and progesterone, and opposite changes in serum prostaglandin E2 and norepinephrine levels, suggesting that EA may regulate neuroendocrine signals of the HPO axis to restore hormonal balance.[52] Moreover, EA can enhance reproductive traits by modulating sex hormone levels and the activity of the HPO axis in PCOS rats. The gene discussed is GNRH1; the disease is polycystic ovary syndrome.