Excess of leptin inhibits hypothalamic KiSS-1 expression in pubertal mice.
10.3345/kjp.2012.55.9.337
- Author:
Sung Yeon AHN
1
;
Sei Won YANG
;
Hee Jae LEE
;
Jong Seon BYUN
;
Ji Yeon OM
;
Choong Ho SHIN
Author Information
1. Department of Pediatrics, Kangwon National University School of Medicine, Chuncheon, Korea.
- Publication Type:Original Article
- Keywords:
Leptin;
KiSS-1;
Gonadotropin-releasing hormone;
Luteinizing hormone;
Puberty
- MeSH:
Aluminum Hydroxide;
Animals;
Axis, Cervical Vertebra;
Carbonates;
Female;
Gene Expression;
Gonadotropin-Releasing Hormone;
Humans;
Leptin;
Luteinizing Hormone;
Mice;
Puberty;
RNA, Messenger
- From:Korean Journal of Pediatrics
2012;55(9):337-343
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Leptin has been considered a link between metabolic state and reproductive activity. Defective reproductive function can occur in leptin-deficient and leptin-excessive conditions. The aim of this study was to examine the effects of centrally injected leptin on the hypothalamic KiSS-1 system in relation to gonadotropin-releasing hormone (GnRH) action in the initial stage of puberty. METHODS: Leptin (1 microg) was injected directly into the ventricle of pubertal female mice. The resultant gene expressions of hypothalamic GnRH and KiSS-1 and pituitary LH, 2 and 4 hours after injection, were compared with those of saline-injected control mice. The changes in the gene expressions after blocking the GnRH action were also analyzed. RESULTS: The basal expression levels of KiSS-1, GnRH, and LH were significantly higher in the pubertal mice than in the prepubertal mice. The 1-microg leptin dose significantly decreased the mRNA expression levels of KiSS-1, GnRH, and LH in the pubertal mice. A GnRH antagonist significantly increased the KiSS-1 and GnRH mRNA expression levels, and the additional leptin injection decreased the gene expression levels compared with those in the control group. CONCLUSION: The excess leptin might have suppressed the central reproductive axis in the pubertal mice by inhibiting the KiSS-1 expression, and this mechanism is independent of the GnRH-LH-estradiol feedback loop.
