Resveratrol Supplementation in Obese Pregnant Rats Improves Maternal Metabolism and Prevents Increased Placental Oxidative Stress

Abstract

Maternal obesity (MO) causes maternal and fetal oxidative stress (OS) and metabolic dysfunction. We investigated whether supplementing obese mothers with resveratrol improves maternal metabolic alterations and reduces OS in the placenta and maternal and fetal liver. From weaning through pregnancy female Wistar rats ate chow (C) or a high-fat diet (MO). One month before mating until 19 days’ gestation (dG), half the rats received 20 mg resveratrol/kg/d orally (Cres and MOres). At 19dG, maternal body weight, retroperitoneal fat adipocyte size, metabolic parameters, and OS biomarkers in the placenta and liver were determined. MO mothers showed higher body weight, triglycerides and leptin serum concentrations, insulin resistance (IR), decreased small and increased large adipocytes, liver fat accumulation, and hepatic upregulation of genes related to IR and inflammatory processes. Placenta, maternal and fetal liver OS biomarkers were augmented in MO. MOres mothers showed more small and fewer large adipocytes, lower triglycerides serum concentrations, IR and liver fat accumulation, downregulation of genes related to IR and inflammatory processes, and lowered OS in mothers, placentas, and female fetal liver. Maternal resveratrol supplementation in obese rats improves maternal metabolism and reduces placental and liver OS of mothers and fetuses in a sex-dependent manner.

Maternal high-fat diet decreases milk endocannabinoids with sex-specific changes in the cannabinoid and dopamine signaling and food preference in rat offspring

“…These data corroborate our previous results showing increased total body fat but not body weight of the dams before mating (23). In contrast, the literature mainly shows that HF diet increases body weight, adiposity, glycemia, dyslipidemia, insulinemia and leptinemia in female rats prior pregnancy, and several serum alterations last until weaning (46)(47)(48)(49). An important characteristic of the present study is that the HF diet used is isocaloric in comparison to the control diet (~3.9 kcal/g), while most of the studies published in the literature are performed using a high-fat and hypercaloric diet (over 5 kcal/g).…”

Nurturing through Nutrition: Exploring the Role of Antioxidants in Maternal Diet during Pregnancy to Mitigate Developmental Programming of Chronic Diseases

“…In addition, oral supplementation of resveratrol in HFD-induced obese mothers decreased the expression of hepatic genes encoding for proteins involved both in glycolysis (i.e., Glucose-6-phosphate dehydrogenase (G-6-PDH), Phosphoenolpyruvate carboxykinase (PEPCK)) and in inflammation (i.e., IL-6), where it decreased the concentration of a DNA oxidation marker (8-Oxo-2 -deoxyguanosine-8-oxo-dG) and decreased the nitrotyrosine immunostained area in comparison with the MO group. These results suggest that resveratrol attenuated insulin resistance mechanisms, inflammatory processes, and oxidative stress in the maternal liver [144]. At 19 days of gestation, in the placental tissue, resveratrol supplementation in obese mothers carrying male fetuses decreased the levels of the lipid peroxidation biomarker (MDA) in comparison with the MO group, while for female fetuses, ROS levels were decreased along with SOD increased activity [144].…”

Programming Mechanism of Adipose Tissue Expansion in the Rat Offspring of Obese Mothers Occurs in a Sex-Specific Manner

“…There is now compelling evidence that environmental factors, such as inadequate maternal nutrition during pregnancy and/or in early neonatal life, may increase offspring’s susceptibility to developing type 2 diabetes, hypertension, and obesity [ 32 , 33 , 34 , 35 ]. We previously reported that obese mothers show metabolic dysfunction at 19 days of gestation [ 36 ], at the end of lactation [ 2 ] and that milk production and the % of water and carbohydrate content were lower in obese mothers, whereas milk leptin, total fat, arachidonic acid and monosaturated fatty acids were higher, with no changes in protein content [ 37 ] explaining the adverse metabolic outcomes of offspring. However, in many studies, sex differences in offspring are often overlooked as a significant variable in disease development.…”