title: Sensitivities of mRNA expression levels of Kiss1 and its receptor, Kiss1r, to nutritional status are changed during the developmental period in female rats.
abstract: Decreased activity of kisspeptin, the product of the hypothalamic Kiss1 gene, is the major cause of the suppression of reproductive function in subnutritional conditions. The sensitivities of the endocrine and the hypothalamic neuronal systems to nutritional status develop during the neonatal period. We examined the developmental changes in the sensitivity of hypothalamic mRNA expression of Kiss1 and its receptor, Kiss1r, to nutritional status in female rats. Kiss1 mRNA expression was reduced by 24 h food deprivation (24 h FD) at postnatal day 25, but not at postnatal day 5 or 15. Kiss1r mRNA expression was reduced by the 12 or 24 h FD at postnatal days 5 and 25, but not at postnatal day 15. Kiss1r mRNA level was found to be correlated with the plasma leptin level, and the administration of leptin, which increased the serum leptin concentration above the physiological range, restored the acute FD-induced suppression of Kiss1r mRNA expression. These data suggest that the hypothalamic Kiss1 and Kiss1r mRNA expression is differentially affected by the nutritional condition at different age points. It is speculated that the sensitivity of Kiss1 mRNA, which is expressed in kisspeptin neuron, to nutritional status develops during the neonatal period. On the other hand, it seems that the sensitivity of Kiss1r mRNA, which is expressed in GnRH neuron, to nutritional status has been already established during the early neonatal period. These data also show that hypoleptinemia plays a role in the reduction of hypothalamic Kiss1r mRNA expression under subnutritional conditions.
authors.affiliation: Department of Obstetrics and Gynecology, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto-Cho, Tokushima 770-8503, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Iwasa
authors.forename: Toshiya
authors.initials: T
authors.lastname: Matsuzaki
authors.forename: Masahiro
authors.initials: M
authors.lastname: Murakami
authors.forename: Riyo
authors.initials: R
authors.lastname: Kinouchi
authors.forename: Ganbat
authors.initials: G
authors.lastname: Gereltsetseg
authors.forename: Shinobu
authors.initials: S
authors.lastname: Fujisawa
authors.forename: Akira
authors.initials: A
authors.lastname: Kuwahara
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Yasui
authors.forename: Minoru
authors.initials: M
authors.lastname: Irahara
mesh_terms: D000818:Animals; D005260:Female; D005508:Food Deprivation; D018507:Gene Expression Regulation, Developmental / Q000502:physiology*; D007987:Gonadotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D007031:Hypothalamus / Q000378:metabolism; D059648:Kisspeptins; D020738:Leptin / Q000494:pharmacology; D009752:Nutritional Status / Q000502:physiology*; D011506:Proteins / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D043562:Receptors, G-Protein-Coupled / Q000235:genetics / Q000378:metabolism*; D000074502:Receptors, Kisspeptin-1
chemical_list: C491406:Kiss1 protein, rat; C492247:Kiss1r protein, rat; D059648:Kisspeptins; D020738:Leptin; D011506:Proteins; D012333:RNA, Messenger; D043562:Receptors, G-Protein-Coupled; D000074502:Receptors, Kisspeptin-1; D007987:Gonadotropin-Releasing Hormone