Changes in gut-brain axis parameters in adult rats of both sexes with different feeding pattern that were early nicotine-exposed.

Nicotine is an endocrine disruptor and imprinting factor during breastfeeding that can cause food intake imbalance in the adulthood. As nicotine affects the intestinal microbiota, altering the composition of the bacterial communities and short-chain fatty acids (SCFAs) synthesis in a sex-dependent manner, we hypothesized that nicotine could program the gut-brain axis, consequently modifying the eating pattern of adult male and female rats in a model of maternal nicotine exposure (MNE) during breastfeeding. Lactating Wistar rat dams received minipumps that release 6 mg/kg/day of nicotine (MNE group) or saline for 14 days. The progeny received standard diet from weaning until euthanasia (26 weeks of age). We measured: in vivo electrical activity of the vagus nerve; c-Fos expression in the nucleus tractus solitarius, gastrointestinal peptides receptors, intestinal brain-derived neurotrophic factor (BDNF), SCFAs and microbiota. MNE females showed hyperphagia despite normal adiposity, while MNE males had unchanged food intake, despite obesity. Adult MNE offspring showed decreased Bacteroidetes and increased Firmicutes, Actinobacteria and Proteobacteria. MNE females had lower fecal acetate while MNE males showed higher vagus nerve activity. In summary nicotine exposure through the milk induces long-term intestinal dysbiosis, which may affect eating patterns of adult offspring in a sex-dependent manner.

Effects of maternal bisphenol A on behavior, sex steroid and thyroid hormones levels in the adult rat offspring.

AIMS: Bisphenol A (BPA), an endocrine disruptor used in industrial applications, has been detected in both placenta and milk. We studied the effects of BPA exposure during pregnancy and lactation on body composition, palatable food intake, biochemical, hormonal and behavioral profiles of young and adult Wistar rat offspring. MAIN METHODS: Female rats were divided into: control, BPA10 (10 µg/kg/day) and BPA50 (50 µg/kg/day). BPA was administered by gavage to dams from gestation until the end of lactation. Euthanasia occurred at weaning [postnatal day (PN) 21] or adulthood (PN180). KEY FINDINGS: At weaning, BPA10 female pups had higher plasma cholesterol and triacylglycerol. BPA10 male pups showed lower plasma T3. BPA10 pups of both sexes had higher plasma progesterone, testosterone and estradiol. At adulthood, females of both BPA groups had lower food intake and higher insulinemia, whereas males had lower visceral fat, lower progesterone and testosterone concentrations. BPA10 females and males had lower T4 levels, while only males showed lower estradiol. BPA50 females showed lower fat mass, higher lean mass and lower corticosteronemia, while males had lower food intake. In the feeding study, BPA10 males ate more fat at 30 min, while BPA10 females and males ingested less fat after 12 h. BPA10 females showed hyperactivity while both groups showed less exploration. SIGNIFICANCE: Maternal exposure to BPA during gestation and lactation, even at low doses, induces life-long changes in the regulation of metabolic homeostasis of the progeny, affects sex steroids and thyroid hormones levels, compromises behavior, but does not lead to obesity or dyslipidemia.