Interaction of Programmed Obesity and Postnatal High Fat Diet but Not (-)-Epicatechin Treatment Modifies Muscle Atrophy Proteins Levels in Male Wistar Rats.

Abstract

We determine whether the offspring of obese mothers and a postnatal high-fat diet (HFD) modify protein levels related to muscle synthesis (p70S6K-alpha) or atrophy (Murf and MAFbx), and if the administration of (-)-epicatechin (Epi) can modify these alterations. We hypothesized that the ubiquitin ligases Murf and MAFbx would be increased in the obesogenic context, either by in utero obesogenic environment or by a postnatal high-fat diet, while the p70S6K-alpha kinase and its activation might be decreased. Eight groups of six male Wistar offspring formed eight experimental groups: control (C), control fed with HFD (CHFD), maternal obesity (MO), maternal obesity fed with HFD (MOHFD), and the groups with Epi intervention: C+Epi long, CHFD+Epi long, MO+Epi long and MOHFD+Epi long. By Western blot, we evaluated the Epi effect on the Murf, MAFbx, and p70S6K-alpha proteins in gastrocnemius and soleus tissues. The Murf level increased 2.59-fold in CHFD vs C group and 2.62-fold for MOHFD vs C group (p = 0.049 and p = 0.048, respectively) in gastrocnemius tissue. In soleus tissue, we observed an increase of MAFbx (1.52-fold) for the MOHFD group versus the C group (p = 0.049). Epi treatment did not modify any protein expression. In conclusion, we found an increase in the Murf1 protein levels in gastrocnemius tissue of the direct model of obesity; as well, we observed an increase of the Murf1 in gastrocnemius and of the MAFbx in soleus muscles in the group of rats obese by programming and fed postnatally with a high-fat diet (doble stimulus). In addition, since obesity could cause muscle atrophy, which results in impaired muscle function, it would be relevant in future research to evaluate these signaling pathways in animals of different ages in order to search for markers of the progression of diseases such as sarcopenia obesity.