An early-life adverse environment has been involved in the susceptibility to different diseases in adulthood such as mental disorders, diabetes and obesity. We analyzed the effects of a high-fat-sucrose diet (HFS) for 35 days in adult female rats, which had experienced 180 minutes daily of maternal separation (MS) during lactancy. Changes in the obesity phenotype, biochemical profile, glucocorticoid metabolism biomarkers, and the expression of different obesity- and glucocorticoid metabolism-related genes were analyzed in periovaric adipose tissue. HFS intake increased body weight, adiposity and serum leptin levels, while MS decreased fat pad masses but only in rats fed HFS. MS reduced insulin resistance markers but only in chow-fed rats. Corticosterone and estradiol serum levels did not change in this experimental model. A multiple gene expression analysis revealed that the expression of Adiponutrin (Adpn) was increased due to MS, and an interaction between HFS diet intake and MS was observed in the mRNA levels of Leptin (Lep) and Peroxisome proliferator-activated receptor gamma coactivator 1 alpha (Ppargc1a). These results revealed that early-life stress produces a different response to an HFS diet later in life involving different phenotype and transcriptomic changes.
- Received November 9, 2011.
- Accepted July 1, 2012.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.