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- How does kisspeptin regulate the preovulatory LH surge?
Kisspeptin is synthesized in both, arcuate nucleus (KNDy neurons) and AVPV
nuclei (Kiss-1 neurons). However, kisspeptin from KNDy neurons is responsi-
ble for the initiation of puberty, whereas kisspeptin from Kiss-1 neurons is
involved in preovulatory LH surge. This effect is mediated by the stimulatory
effect of estrogen at Kiss-1 neurons present in AVPV nuclei. On the contrary,
AVPV nuclei are devoid of Kiss-1 neurons in males.
- What is the role of leptin in the initiation of puberty?
It has been shown that a critical body weight/body fat is essential for the onset
of puberty. This is evidenced by the presence of delayed/absent puberty in
girls with low body fat and early puberty in obese girls. Adipose tissue signals
to hypothalamus through the adipokine leptin, which stimulates KNDy
neurons. This results in the release of kisspeptin, which in turn activates HPG-
axis. The key role of leptin in the induction of puberty is evidenced by the
occurrence of isolated hypogonadotropic hypogonadism in individuals with
congenital leptin deficiency and initiation of puberty in these individuals with
recombinant leptin therapy. Despite these evidences, leptin is considered to
have a permissive role, rather than a primary role as evidenced by timely onset
of puberty in patients with congenital generalized lipodystrophy, who are defi-
cient in leptin.
- What is “mini-puberty”?
Reactivation of Hypothalamic–pituitary–gonadal (HPG) axis during neonatal
period occurs as a result of withdrawal of inhibitory effect of placental estrogen
on HPG-axis and is termed as “mini-puberty.” It is characterized by postnatal
surge of gonadotropins and sex steroids that initiate at approximately second
week of life. In boys, gonadotropins and testosterone peak at 3 months and
decline by 6–9 months of age. In girls, FSH and LH peak at 3 months; although
LH levels decline by 6–9 months of age, FSH remains elevated for about
3–4 years of age. Serum estradiol levels widely fluctuate during mini-puberty
in girls, whereas serum testosterone is stable in boys. The wide fluctuation in
serum estradiol during mini-puberty is possibly due to cyclical maturation of
ovarian follicles (Fig. 7.3).
7 Delayed Puberty