Maternal lactation proves crucial for mammals’ nutrition during their early development, influencing the development of adult physiological mechanisms. Its premature termination has been associated with several disorders, but these have been primarily documented in males, when they are most prevalent in women. Therefore, we subjected adult female Wistar rats to Early Weaning through maternal separation at age 15 days to acute alimentary stress in the form of visual and olfactory exposition to a cafeteria diet sans consumption for 22 days. We measured standard diet intake and water intake daily and cafeteria diet intake every 7 days. Additionally, we evaluated anxiety using the elevated plus maze and measured body weight in similar intervals. Results showed less consumption of the cafeteria diet among Early Weaning rats on day 2 and more time spent in the maze’s central area by the Early Weaning rats during the basal evaluation and in the maze’s open arms by control rats on day 7 when compared to the same group’s basal time. No other significant differences were found. These results show the importance of determining the impact that female steroidal gonadal hormones such as estradiol have upon feeding behavior and anxiety and determining to what degree these parameters are influenced by hormonal action.

Background/Objectives: Diets high in simple carbohydrates and saturated fats, commonly consumed in Westernized countries, have been linked to a greater predisposition to metabolic disorders, which are partly attributed to oxidative stress. This study aimed to investigate the impact of an obesogenic diet consumed during the pregnancy and lactation periods on hepatic metabolism and REDOX balance in rats. Methods: Sixteen pregnant Wistar rats were divided into two groups: control (CD), which received a vivarium diet, and obesogenic (OD), which received an obesogenic diet (high-fat diet plus condensed milk), from early pregnancy to late lactation. Thirty-six hours after weaning, the rats were euthanized, and blood, adipose tissue, and liver samples were collected for analysis. Results: These results demonstrate that exposure to an obesogenic diet during pregnancy and lactation in rats leads to adverse changes in hepatic metabolic, inflammatory, and REDOX balance. This experimental animal model serves as a valuable tool for investigating the mechanisms of metabolic dysfunction associated with diets that mimic human eating habits. However, it is essential to note that these findings pertain to an experimental model and therefore require validation in clinical studies to confirm their relevance and applicability in human health. Conclusions: The consumption of an obesogenic diet during pregnancy and lactation in rats induces adverse alterations in hepatic metabolic, inflammatory, and redox homeostasis. This animal model helps investigate the mechanisms of metabolic dysfunctions associated with human dietary habits. However, these findings still need to be confirmed in clinical studies to verify their relevance in humans.

Tryptophan, an essential amino acid in mammals obtained from the diet, is influenced by maternal diet, which impacts early life and development of offspring. This is studied under the Developmental Origins of Diseases and Health (DOHaD) concept, so factors from conception to early childhood affect health and disease susceptibility. Tryptophan is metabolized mainly through two pathways: serotonin (5-HT) and kynurenine. The kynurenine pathway, active in the brain, gut, liver, and placenta, breaks down over 95% of tryptophan and plays roles in inflammation, neurotransmission, immune responses, and immune modulation during pregnancy. The serotonin pathway uses up to 5% of Tryptophan, mainly in the gut, adipose tissues, pancreatic cells, and central nervous system, and regulates responses to environmental changes, including sleep, cognition, and feeding behavior. Key enzymes in these pathways include Trp-2,3-dioxygenase (TDO), indoleamine-2,3-dioxygenase (IDO) type1 (IDO1), and type 2 (IDO2) (kynurenine pathway), and tryptophan hydroxylase type 1 (TPH1) and type 2 (TPH2), serotonin pathway. The fetus-placental unit manages tryptophan metabolism. Serotonin and kynurenine are crucial for placental health and fetal development. Serotonin adjusts placental blood volume and aids neurodevelopment. Kynurenine metabolites protect the fetus from maternal immunity and offer initial neuroprotection. At birth, infants switch from placental nutrients to breast milk, rich in tryptophan and protective bioactive molecules. Tryptophan, solely from breast milk, is crucial for infants. Its levels are high in newborns (first three weeks, 2-4 times higher than in adults), gradually declining to adult levels by the fourth week. The highlights the importance of tryptophan for the serotonin and kynurenine pathways in fetuses, newborns and babies applied to the DOHaD concept.