Obesity phenotype induced by high-fat diet leads to maternal-fetal constraint, placental inefficiency, and fetal growth restriction in mice.

The aim of this study was to investigate certain parameters regarding the maternal-fetal outcomes in a diet-induced obesity model. Obese, glucose-intolerant females who were exposed to a high-fat diet prior to pregnancy had lower placental efficiency and lower birth weight pups compared to the controls. Simple linear regression analyses showed that maternal obesity disrupts the proportionality between maternal and fetal outcomes during pregnancy. Maternal obesity is correlated with fetal outcomes, perhaps because of problems with hormonal signaling and exacerbation of inflammation in the maternal metabolic environment. The maternal obese phenotype altered the thickness of the placental layer, the transport of fatty acids, and the expression of growth factors. For example, lower expression of epidermal growth factor receptor (EGFR) mRNA in the obesity-prone group may have contributed to the rupture of the placental layers, leading to adverse fetal outcomes. Furthermore, maintenance of maternal glucose homeostasis and overexpression of placental growth factor (PGF) in the obesity-resistant group likely protected the placenta and fetuses from morphological and functional damage.

Maternal soy protein isolate diet during lactation programs deleterious effects on hepatic lipid metabolism, atherogenic indices, and function of adrenal in adult rat offspring.

The benefits of consuming soy and its protein have been reported in many studies. However, its phytoestrogen content raises concerns about consumption during lactation and gestation We therefore examined the effects of soybean or soy protein isolate on the parameters-related cardiovascular pathophysiology in lactating mothers and their offsprings at weaning and adulthood. Lactating rats were divided: casein control (C); soy protein isolate (SPI); and soybean (S). At weaning, half of the litter received commercial ration up to 150 days. The levels of 17-ß-estradiol and superoxide dismutase were low in the S mothers. For the SPI mothers, we observed a reduction of thiobarbituric acid reactive substances (TBARS). At weaning, atherogenic indices [1 = total cholesterol (TC)/HDL; 2 = LDL/HDL; 3 = TC-HDL/HDL)] decreased in the S and SPI offsprings compared to the casein control group; TBARS and antioxidant enzymes increased in the S offspring, while reduced/oxidized glutathione ratio increased in the SPI offspring, indicating lower oxidative stress. In adulthood, the SPI offspring showed an increase in liver cholesterol and atherogenic index 1 and 3 (vs. C and S) and 2 (vs. S). In addition, we found a decrease in catecholamines in the adrenal medulla and an increase in caffeine-stimulated secretion, but tyrosine hydroxylase expression remained constant. Maternal consumption of SPI during lactation worsened atherogenic indices of the offsprings in adulthood, which was associated with increased liver cholesterol and decreased catecholamines in the adrenal medulla. Soy consumption had no consistent long-term effects on the evaluated parameters compared to casein consumption. The data suggest that the consumption of SPI during lactation should be done with caution.

Maternal soybean diet during lactation alters breast milk composition and programs the lipid profile in adult male rat offspring.

PURPOSE: To evaluate the effects of maternal dietary soybean during lactation on the milk composition, body composition, lipid profile and glucose homeostasis of dams and offspring at weaning (21 days) and adulthood (150 days). METHODS: Lactating rats were divided into: casein control (C): casein diet; soy (S): soybean diet; soy oil control (SOC): casein diet, but with fat content similar to the S group. RESULTS: At 21 days, S mothers showed lower estradiol, total cholesterol (TC), low-density lipoprotein cholesterol (LDL) and triglycerides (TG) in serum; and lower TC and TG in milk. The S offspring had lower body weight, body fat mass, TC, LDL, hyperleptinemia and hypertriglyceridemia. At 150 days, S offspring presented higher total mineral content and lower TC (v. SOC) and LDL (v. C and SOC), and hyperinsulinemia with lower glycemia v. SOC group, which had lower insulinemia with higher glycemia, TC and LDL. CONCLUSIONS: Maternal intake of soybeans in lactation changes the lipid content of breast milk and programmed offspring for phenotype of the lower metabolic risk, with lower serum TC and LDL, and seems to protect the progeny of alterations in glucose metabolism despite the higher lipid content. The difference in fat content of breast milk and the higher isoflavones content of soy diet are possible imprinting factors that could program the offspring.