Maternal obesogenic diet combined with postnatal exposure to high‐fat diet induces metabolic alterations in offspring

Abstract

Maternal obesity has been shown to impact the offspring health during childhood and adult life. This study aimed to evaluate whether maternal obesity combined with postnatal exposure to an obesogenic diet could induce metabolic alterations in offspring. Female CD1 mice were fed a control diet (CD, 11.1% of energy from fat) or with a high‐fat diet (HFD, 44.3% of energy from fat) for 3 months. After weaning, pups born from control and obese mothers were fed with CD or HFD for 3 months. Both mothers and offspring were weighted weekly and several blood metabolic parameters levels were evaluated. Here, we present evidence that the offspring from mothers exposed to a HFD showed increased acetylation levels of histone 3 on lysine 9 (H3K9) in the liver at postnatal Day 1, whereas the levels of acetylation of H4K16, dimethylation of H3K27, and trimethylation of H3K9 showed no change. We also observed a higher perinatal weight and increased blood cholesterol levels when compared to the offspring on postnatal Day 1 born from CD‐fed mothers. When mice born from obese mothers were fed with HFD, we observed that they gained more weight, presented higher blood cholesterol levels, and abdominal adipose tissue than mice born to the same mothers but fed with CD. Collectively, our results point toward maternal obesity and HFD consumption as a risk factor for epigenetic changes in the liver of the offspring, higher perinatal weight, increased weight gain, and altered blood cholesterol levels.

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

“…Therefore, postnatal interventions with bioactive compounds, as the flavonoid (−)‐epicatechin, may be a strategy to reduce those comorbidities associated with obesity [6, 7]. Bariani et al [15] observed a higher body weight and abdominal adipose tissue in offspring mice of maternal obese mothers postnatally fed with an HFD versus offspring exposed to an HFD but born to mothers who received a chow diet. In addition, Sertiea et al [16] showed that rats fed with HFD and descendants of an obesity model had the highest calorie intake, total fat, and percentage of body fat mass, followed by the offspring of obese mothers that consumed a chow diet in comparison with the offspring of the control groups.…”

“…Regarding our results, we observed that the offspring of maternal obesity and postnatally fed with HFD (MOHF group) and the descendant of maternal obesity but with chow diet (CHF) had a higher total fat tissue, retroperitoneal fat, mesenteric fat, pancreatic fat, and adiposity visceral index in comparison with the control groups (C and MO groups), although the offspring of the MOHF group had a significantly higher food intake compared with the offspring of a direct model of obesity (CHF group). Like it has been proposed, maternal HFD increases hedonic feeding in the offspring [32], due to disorders in normal fetal neurodevelopment that could impact on food intake behavior later in life, predisposing the offspring to food‐related impulsivity and overconsumption of energy‐dense food [15]. In addition to a postweaning overfeeding of their pups, the obesogenic intrauterine environment has a significant deleterious effect on their health because they present exaggerate adiposity [33], as we observed in the offspring of the MOHF group.…”

“…Likewise, it has been shown in a rodent model of maternal obesity combined with a postnatal high-fat diet (HFD), in their offspring, to induce a more significant increase in body weight and fat tissue [15,16], as well as modifications in the morphometry and histomorphometry of the bone promoting adipocyte accumulation offspring bone marrow [17].…”

Elevated RIF1 participates in the epigenetic abnormalities of zygotes by regulating histone modifications on MuERV-L in obese mice

“…Western blotting was performed as described previously (Bariani et al 2020 ; Han et al 2018 ). A total of 100 MII oocytes or embryos were added to 2 × SDS sample buffer, incubated at 95 °C for 5 min and then frozen at -30 °C until further use.…”

“…Obesity not only is associated with increased risks of almost every common complication of pregnancy, but also plays a direct role in the transgenerational transmission of an obesity or diabetes risk. Increasing evidence suggests that offspring of obese mothers are at increased risk of obesity (Bariani et al 2020 ; Daxinger and Whitelaw 2012 ; Keleher et al 2018 ), impaired glucose tolerance (Dunn and Bale 2009 ; Godfrey et al 2017 ), and other facets of the metabolic syndrome (Catalano and Ehrenberg 2006 ; Volpato et al 2012 ). The increased risks of metabolic abnormalities in offspring are probably associated with epigenetic abnormalities in maternal oocytes (Ou et al 2019 ).…”