title: Delayed puberty in prenatally glucocorticoid administered female rats occurs independently of the hypothalamic Kiss1-Kiss1r-GnRH system.
abstract: Intrauterine growth retardation (IUGR) is an important risk factor for the pathogenesis of diseases after birth. Long-lasting alterations in the structure and function of tissues and the neuroendocrine system, which are known as 'programming effects', increase the risks of these diseases. To investigate the pathophysiology of programming effects, several kinds of IUGR rodent models have been used in experiments. Sexual maturation and the onset of puberty are delayed in these models. We have previously reported that decreased action of hypothalamic kisspeptin, which is a positive regulator of GnRH, contributes to the delayed onset of puberty in undernutrition-induced IUGR rats. The aim of this study was to evaluate whether the hypothalamic Kiss1-Kiss1r-GnRH system is also altered in dexamethasone-induced IUGR rats. Compared with offspring from an untreated mother (control), offspring from a dexamethasone administered mother (DEX) showed a significant reduction in body weight throughout the experimental period (from birth to the prepubertal period) and the delayed onset of puberty. There were no significant differences between the control and DEX groups with regard to their hypothalamic Kiss1, Kiss1r, GnRH, CRH, NPY and POMC mRNA levels during the experimental period or their serum LH, FSH, or leptin concentrations at postnatal day 28 or vaginal opening (VO). Compared with the control, DEX showed significantly lower ovarian weight at postnatal day 28, but not at VO. These results suggested that the delayed onset of puberty induced by maternal dexamethasone administration would occur independently of hypothalamic Kiss1-Kiss1r-GnRH system.
authors.affiliation: Department of Obstetrics and Gynecology, The University of Tokushima Graduate School, Institute of Health Biosciences, 3-18-15 Kuramoto-Cho, Tokushima 770-8503, Japan. takeshi1@clin.med.tokushima-u.ac.jp
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: Satoshi
authors.initials: S
authors.lastname: Yamamoto
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; D003907:Dexamethasone / Q000494:pharmacology; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology; D005938:Glucocorticoids / Q000494:pharmacology*; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism*; D007031:Hypothalamus / Q000187:drug effects*; D059648:Kisspeptins; D011247:Pregnancy; D011506:Proteins / Q000378:metabolism*; D011628:Puberty, Delayed / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism*; D000074502:Receptors, Kisspeptin-1
chemical_list: D005938:Glucocorticoids; C491406:Kiss1 protein, rat; C492247:Kiss1r protein, rat; D059648:Kisspeptins; D011506:Proteins; D043562:Receptors, G-Protein-Coupled; D000074502:Receptors, Kisspeptin-1; D007987:Gonadotropin-Releasing Hormone; D003907:Dexamethasone