Kisspeptin neurons in the hypothalamus play a central role in GnRH pulse regulation. In hypothalamic amenorrhea (functional hypothalamic amenorrhea, FHA) due to energy deficit or stress, kisspeptin neuronal activity is:

• A Decreased, resulting in reduced GnRH pulse frequency and low gonadotropins ✓
• B Increased, driving excess GnRH secretion and leading to elevated FSH
• C Unchanged; FSH is selectively suppressed by elevated cortisol
• D Decreased FSH only; LH pulsatility is preserved through leptin signaling

Explanation

Kisspeptin (product of KISS1 gene) neurons in the arcuate nucleus (KNDy neurons co-expressing kisspeptin, neurokinin B, and dynorphin) are the master regulators of GnRH pulse generation. In functional hypothalamic amenorrhea, low energy availability, elevated cortisol, and low leptin suppress kisspeptin neuronal activity, reducing GnRH pulse frequency and amplitude—leading to low LH and FSH and subsequent hypogonadotropic hypogonadism. This is a reversible adaptive response. Leptin normally promotes kisspeptin release; in FHA, low leptin (from low adiposity/energy stores) is a key suppressor. Kisspeptin analogues are currently under investigation as diagnostic tools and potential therapeutic agents for FHA and hypothalamic infertility.

Reference: Shaw's Textbook of Gynaecology, 17th ed.

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Written and medically reviewed by the StethoPrep medical team.