Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 GP13.04 | DOI: 10.1530/endoabs.37.GP.13.04


1University of Cordoba, Cordoba, Spain; 2Instituto Maimonides de Investigacion Biomedica de Cordoba (IMIBIC), Cordoba, Spain; 3CIBERobn, Cordoba, Spain; 4University of Santiago de Compostela, Santiago de Compostela, Spain.


While female fertility is known to be sensitive to conditions of low body fuel reserves, the reproductive consequences of persistent energy excess remain ill defined. Yet, the pandemic proportions of obesity, and its potential impact on the gonadotropic axis, call for a better understanding of this phenomenon. Alike, the influence of ovarian hormones on the pathophysiology of obesity and its complications merits further investigation. In this work, we aimed to elucidate the metabolic and reproductive/gonadotropic impact of various obesogenic insults in the female rat, with special attention to the influence of the loss of ovarian secretion, as model of menopause. To this end, we implemented a series of neuroendocrine studies on the metabolic and gonadotropic consequences of sequential obesogenic insults, namely, postnatal over-nutrition (SL) and high fat diet (HFD) after weaning, in gonadal-intact and ovariectomized (OVX) female rats. In young (4-mo) cyclic females, SL or HFD caused similar increases in body weight; yet, only HFD evoked additional metabolic perturbations, some of which were worsened by precedent SL. In addition, HFD caused a concomitant decrease in LH and estradiol levels, and suppressed Kiss1 expression in the arcuate nucleus (ARC) of the hypothalamus in 4-mo females, while persistent HFD up to 10-mo induced also suppression of LH responses to kisspeptin-10. OVX caused a severe and rapid deterioration of the metabolic profile, with overweight, increased energy intake and deregulation of leptin and glucose/insulin levels; effects whose magnitude was similar, if not higher than HFD. Summation of previous obesogenic insults maximally increased body weight, basal leptin, insulin and glucose levels, and glucose intolerance. Yet, OVX obliterated the inhibitory effects of overweight/ HFD on gonadotropin levels and ARC Kiss1 expression, which were heightened due to the loss of negative feedback. In sum, our study characterizes the metabolic and gonadotropic effects of sequential exposures to obesogenic insults, and their interactions with ovarian secretions. Our data document the deleterious consequences of overweight on the female gonadotropic axis, via impairment of Kiss1 system, and substantiate the dramatic impact of OVX, as menopausal model, on the metabolic profile, especially when combined with preceding obesogenic insults.

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