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

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.

Developmental programming-ageing effects in muscle strength of obese rat offspring in a sex-dependent manner.

Maternal obesity programs the offspring to metabolic dysfunction. However, the effects of maternal obesity on skeletal muscle programming and ageing have been little explored. To determine if maternal obesity is a detriment to the progress of age-related muscle strength loss in the offspring (F), we evaluated the indicators of muscle strength, adiposity, and metabolism at young adult and senior adult ages of maternal obesity F1 (MOF) males and females from a high-fat diet-induced maternal obesity model in rat.

Obesity-Induced Memory Deficits in Female Rats Are Oestrous Cycle Dependent and Linked to Impaired Brain Kynurenine Pathway Metabolism.

Introduction: Obesity is associated with impaired learning, but the mechanisms underlying this cognitive dysfunction are poorly understood. Moreover, whether obesity-induced learning deficits show sexual dimorphism remains controversial. Females are believed to be protected from cognitive decline by oestrogens.

Sex-differential RXRα gene methylation effects on mRNA and protein expression in umbilical cord of the offspring rat exposed to maternal obesity.

Maternal obesity (MO) induces negative consequences in the offspring development. Adiposity phenotype is associated with maternal diet at early pregnancy and DNA methylation marks in the RXRα promotor at birth. Glucocorticoids play an important role in the regulation of metabolism through the activation of nuclear hormone receptors such as the RXRα protein.

Postnatal exposure to lipopolysaccharide combined with high-fat diet consumption induces immune tolerance without prevention in spatial working memory impairment.

High-fat diet (HFD) consumption has been related to metabolic alterations, such as obesity and cardiovascular problems, and has pronounced effects on brain plasticity and memory impairment. HFD exposure has a pro-inflammatory effect associated with microglial cell modifications in the hippocampus, a region involved in the working memory process. Immune tolerance can protect from inflammation in periphery induced by HFD consumption, when the immune response is desensitized in development period with lipopolysaccharide (LPS) exposure, maybe this previously state can change the course of the diseases associated to HFDs but is not known if can protect the hippocampus's inflammatory response.

(-)-Epicatechin improves body composition of male rats descendant of obese mothers postnatally fed with a high-fat diet.

A combination of maternal obesity and high-fat diet (HFD) in offspring postnatal life has deleterious effects, and (-)-epicatechin (Epi) treatment can reverse these adverse effects. To investigate whether Epi administration can modify fat mass, muscle mass, and bone mass in male rats descended from obese mothers, fed postnatally on an HFD. Male offspring of mothers fed with control diet formed the control group (C), control group with high-fat diet (CHF), and control group with high-fat diet + epicatechin (CHF + Epi).

Maternal DHA Supplementation during Pregnancy and Lactation in the Rat Protects the Offspring against High-Calorie Diet-Induced Hepatic Steatosis.

Maternal supplementation during pregnancy with docosahexaenoic acid (DHA) is internationally recommended to avoid postpartum maternal depression in the mother and improve cognitive and neurological outcomes in the offspring. This study was aimed at determining whether this nutritional intervention, in the rat, protects the offspring against the development of obesity and its associated metabolic disorders. Pregnant Wistar rats received an extract of fish oil enriched in DHA or saline (SAL) as placebo by mouth from the beginning of gestation to the end of lactation.

(-)-Epicatechin reduces adiposity in male offspring of obese rats.

Objective: To determine whether (-)-epicatechin (Epi) could decrease visceral adipose tissue and improve the metabolic profile of male offspring rats, after maternal obesity was induced by a high-fat diet (HFD).

Design: Maternal obesity in albino Wistar rats was induced with a HFD, whereas male offspring were fed with chow diet throughout the study. Eight male offspring per group, from different litters, were randomly assigned to the experimental or to the control groups.