No Kiss1ng by leptin during puberty?

Research output: Contribution to journalComment/debate

Abstract

Leptin exerts a permissive action on puberty by stimulating release of gonadotropin-releasing hormone (GnRH) in the hypothalamus. However, GnRH neurons lack leptin receptor (LepR), indicating that leptin must indirectly regulate these neurons. The Kiss1 gene produces kisspeptins that stimulate GnRH secretion. Because Kiss1 neurons express LepR and inactivation of Kiss1 causes hypogonadotropic hypogonadism, Donato et al., in this issue of the JCI, assessed whether deletion of LepR from Kiss1 neurons would prevent sexual maturation. Unexpectedly, mice lacking LepR in Kiss1 neurons had normal pubertal development and fertility. In contrast, deletion of LepR from the ventral premammillary nucleus, a region of the brain involved in sexual behavior, prevented puberty and fertility. These findings highlight the complex biology of leptin in reproduction.

Original languageEnglish (US)
Pages (from-to)34-36
Number of pages3
JournalJournal of Clinical Investigation
Volume121
Issue number1
DOIs
StatePublished - Jan 4 2011
Externally publishedYes

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Puberty
Leptin Receptors
Leptin
Neurons
Gonadotropin-Releasing Hormone
Fertility
Kisspeptins
Posterior Hypothalamus
Sexual Maturation
Hypogonadism
Sexual Behavior
Hypothalamus
Reproduction
Brain
Genes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

No Kiss1ng by leptin during puberty? / Ahima, Rexford S.

In: Journal of Clinical Investigation, Vol. 121, No. 1, 04.01.2011, p. 34-36.

Research output: Contribution to journalComment/debate

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