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ReprObesity SIGNED

Overweight-induced Hypogonadism as major factor for the generation and/or perpetuation of Metabolic Co-morbidities of Obesity: Contribution of Epigenetic Regulatory Mechanisms

Total Cost €


EC-Contrib. €






Project "ReprObesity" data sheet

The following table provides information about the project.


Organization address
postcode: 14005

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Spain [ES]
 Total cost 158˙121 €
 EC max contribution 158˙121 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2016
 Duration (year-month-day) from 2016-10-01   to  2018-09-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSIDAD DE CORDOBA ES (CORDOBA) coordinator 158˙121.00


 Project objective

Obesity is a global health problem whose prevalence is increasing substantially due to lifestyle changes. This complex medical condition is frequently linked to serious metabolic complications and deregulation of hormonal axes, which lead to perturbed homeostasis in conditions of overweight. Different studies have suggested that obesity is often associated to hypogonadism, a reproductive disorder that might also promote metabolic alterations, thus setting a vicious circle in the generation/perpetuation of obesity co-morbidities. While the targets and molecular mechanisms underlying this phenomenon are still unknown, emerging evidence from experimental models of metabolic stress linked to hypogonadism strongly suggests the potential role of perturbations of hypothalamic Kiss1/NKB neurons. Likewise, the recently identified involvement of epigenetics in the control of Kiss1 expression at puberty, a crucial stage in sexual development that is metabolically gated, suggests also the contribution of these regulatory mechanisms to this phenomenon. In this context, this project aims to elucidate the pathophysiological relevance of epigenetic regulatory mechanisms in obesity-induced hypogonadism and their influence in the generation/ maintenance of the metabolic complications of overweight. To this end, we will characterize the time-course of alterations of key hormonal and epigenetic factors in preclinical models of obesity and will evaluate the contribution of epigenetic modifications in deregulation of hypothalamic Kiss1/NKB neurons in conditions of overweight. In addition, we will analyse the potential role of gonadal steroids in this phenomenon. This project will help to identify the molecular targets and epigenetic mechanisms responsible for the metabolic perturbations linked to obesity-induced hypogonadism, and will aid to define better tools for the treatment of these complications.


year authors and title journal last update
List of publications.
2018 M. J. Vazquez, C. A. Toro, J. M. Castellano, F. Ruiz-Pino, J. Roa, D. Beiroa, V. Heras, I. Velasco, C. Dieguez, L. Pinilla, F. Gaytan, R. Nogueiras, M. A. Bosch, O. K. Rønnekleiv, A. Lomniczi, S. R. Ojeda, M. Tena-Sempere
SIRT1 mediates obesity- and nutrient-dependent perturbation of pubertal timing by epigenetically controlling Kiss1 expression
published pages: , ISSN: 2041-1723, DOI: 10.1038/s41467-018-06459-9
Nature Communications 9/1 2019-04-18

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