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Prepubertal exposure to glucocorticoid delays puberty independent of the hypothalamic Kiss1‐GnRH system in female rats
Author(s) -
Kinouchi Riyo,
Matsuzaki Toshiya,
Iwasa Takeshi,
Gereltsetseg Ganbat,
Nakazawa Hiroshi,
Kunimi Kotaro,
Kuwahara Akira,
Yasui Toshiyuki,
Irahara Minoru
Publication year - 2012
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2012.09.001
Subject(s) - medicine , endocrinology , dexamethasone , glucocorticoid , saline , endocrine system , kisspeptin , hypothalamus , hormone , gonadotropin releasing hormone , leptin , luteinizing hormone , obesity
Secretion of glucocorticoids is widely known as a key endocrine response to stresses. Prenatal dexamethasone administration induces intrauterine growth retardation and delayed onset of puberty in female rats independent of the hypothalamic Kiss1‐gonadotropin‐releasing hormone (GnRH) system. The aim of this study was to evaluate the influence of chronic intracerebroventricular (central, CD) or subcutaneous (peripheral, PD) dexamethasone administration to prepubertal female rats on the onset of puberty and body weight change. Rats administered dexamethasone from day 25 to day 34 (CD and PD) showed significantly reduced body weight gain throughout the experimental period and delayed onset of vaginal opening compared with rats administered saline centrally (CS) or peripherally (PS). At 34 days old, hypothalamic Kiss1r mRNA levels were significantly lower with CD than with CS. No significant differences were seen between rats administered saline and rats administered dexamethasone with regard to hypothalamic Kiss1 , GnRH and NPY mRNA levels or serum LH levels. Serum leptin concentrations were higher in CD and PD than in the controls (CS and PS). These results suggest that the delayed onset of puberty induced by prepubertal dexamethasone administration occurs independent of the hypothalamic Kiss1‐GnRH system.