Abstract
To examine the effects of maternal resveratrol in rats borne to dams with gestational high-fat diet (HFD)/obesity with or without postnatal high-fat diet. We first tested the effects of maternal resveratrol intake on placenta and male fetus brain in rats borne to dams with gestational HFD/obesity. Then, we assessed the possible priming effect of a subsequent insult, male offspring were weaned onto either a rat chow or a HFD. Spatial learning and memory were assessed by Morris water maze test. Blood pressure and peripheral insulin resistance were examined. Maternal HFD/obesity decreased adiponectin, phosphorylation alpha serine/threonine-protein kinase (pAKT), sirtuin 1 (SIRT1), and brain-derived neurotrophic factor (BDNF) in rat placenta, male fetal brain, and adult male offspring dorsal hippocampus. Maternal resveratrol treatment restored adiponectin, pAKT, and BDNF in fetal brain. It also reduced body weight, peripheral insulin resistance, increased blood pressure, and alleviated cognitive impairment in adult male offspring with combined maternal HFD and postnatal HFD. Maternal resveratrol treatment restored hippocampal pAKT and BDNF in rats with combined maternal HFD and postnatal HFD in adult male offspring dorsal hippocampus. Maternal resveratrol intake protects the fetal brain in the context of maternal HFD/obesity. It effectively reduced the synergistic effects of maternal HFD/obesity and postnatal HFD on metabolic disturbances and cognitive impairment in adult male offspring. Our data suggest that maternal resveratrol intake may serve as an effective therapeutic strategy in the context of maternal HFD/obesity.
Highlights
Maternal obesity is a global problem, with over 30% of women at child-bearing age being categorized as obese [1]
Post hoc analysis showed that the maternal high-fat diet (HFD)/obesity (H group) had higher concentration of IL-1β than the maternal rat chow (C group) (p < 0.05); there was no significant difference between the H and maternal HFD/obesity + maternal resveratrol (HR groups) (p > 0.05) (Figure 1B)
One-way analysis of variance (ANOVA) showed a significant difference in interleukin 6 (IL-6) levels among the four groups (p < 0.05)
Summary
Maternal obesity is a global problem, with over 30% of women at child-bearing age being categorized as obese [1]. Obesity in pregnancy is associated with an increased risk of pre-eclampsia, gestational diabetes, miscarriage, premature delivery, and high Cesarean section rate [2]. It is estimated that the economic cost of obesity in pregnancy is greater than USD 100 million annually in the USA [3]. Maternal obesity can cause a cyclical transgenerational transmission of obesity [4]. Epidemiological and experimental studies provide evidence of the long-term deleterious effect of maternal obesity on offspring—the so-called hypothesis of intrauterine programming [5]. Mounting evidence suggests that an intrauterine high-fat environment plays a crucial role in the development of diseases in offspring, such as hypertension, diabetes, and nervous system diseases [6]
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