ECE2016 Eposter Presentations Obesity (69 abstracts)
Intergenerational influence of paternal obesity on metabolic and reproductive health of the offspring: male-preferential impact and potential involvement of Kiss1-mediated pathways
Miguel Ángel Sánchez-Garrido 1, , Francisco Ruiz-Pino 1, , Alexia Barroso 1, , Inmaculada Velasco 1 , Violeta Heras 1 , María Jesús Vázquez 1, , Juan Manuel Castellano 1, , Juan Roa 1, , Leonor Pinilla 1, & Manuel Tena-Sempere 1,
1Department of Cellular Biology, Physiology and Immunology, Univeristy of Córdoba & Maimónides Institute of Biomedical Research of Córdoba (IMIBIC), Córdoba, Spain; 2CIBER Fisiopatologia de la Obesidad y Nutricion (CIBEROBN). Instituto de Salud Carlos III, Córdoba, Spain.
Obesity and its comorbidities are reaching epidemic proportions. Maternal obesity is known to predispose the offspring to metabolic disorders, independently of genetic inheritance. This intergenerational transmission has also been suggested for paternal obesity during the pre-conception stage, as it appears to have a negative impact on the metabolic and reproductive health of the offspring, likely via epigenetic changes in spermatozoa. However, whether paternal obesity sensitizes the offspring to the disturbances induced by high fat diet (HFD) remains poorly defined. We report herein the metabolic and reproductive impact of HFD in the offspring from obese fathers, with special attention to potential sex differences and alterations of hypothalamic Kiss1 system. Lean and extremely obese male rats were mated with lean, virgin female rats; male and female offspring from lean and obese fathers were fed HFD from weaning onwards. At postnatal day 120, the offspring were euthanized and several metabolic and reproductive parameters analyzed. The increase in body weight and leptin levels, but not glucose intolerance, induced by HFD were significantly higher in the male offspring from obese fathers. In contrast, no differences were detected in the female offspring from both paternal groups; actually, glucose intolerance was lower in HFD-fed females from obese fathers. Paternal obesity caused a decrease in LH levels and exacerbated the drop in testosterone caused by HFD, which was associated to reduced testicular expression of key enzymes of testosterone biosynthesis. In addition, LH responses to central kisspeptin-10 administration were suppressed in HFD-fed males from obese fathers. In contrast, paternal obesity did not significantly alter gonadotropin levels in HFD females; yet, LH responses to kisspeptin-10 were dramatically reduced in the female offspring from obese fathers. Our findings suggest that HFD-induced metabolic and reproductive disturbances are exacerbated by paternal obesity, mainly in males, while kisspeptin actions are affected in both sexes.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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