IMPACT OF EARLY-LIFE STRESS IN ADULTS: RELATIONSHIP WITH FEEDING BEHAVIOR AND SYSTEMIC IMMUNE RESPONSE AND METABOLISM

Feeding and stress responses are regulated by the hypothalamus through the melanocortin system (MCS), composed of POMC neurons (satiety), AgRP/NPY neurons (hunger), and melanocortin receptors. The MCS might also modulate cortisol expression and stress-related emotional states, and alterations can affect both food intake and emotional regulation. Early-life stress (ELS) enhances pro-inflammatory immune responses, which may contribute to hypothalamic–pituitary–adrenal axis dysregulation and impaired neural plasticity, potentially affecting stress and feeding circuits. In mice, neuronal circuits from the hypothalamic arcuate nucleus (ARC) mature during the early postnatal period, a critical window of high neuronal plasticity influenced by internal factors such as an increase in circulating leptin (P4–P14), but also by external stimuli. Evidence suggests that stress during this period can modify these circuits and impact feeding and stress responses in adulthood. We investigated whether ELS affects feeding behavior and systemic immune responses and metabolic parameters. Mice underwent maternal separation for 4 h/day (P3–P10) and 8 h/day (P11–P20) and were weaned at P21. Body weight was recorded until P90. At P90, animals were euthanized, and blood was collected to assess immune markers by flow cytometry; corticosterone, leptin and insulin were measured by ELISA in both sexes. ELS significantly decreased weight gain until P21, followed by subsequent normalization. ELS resulted in increased levels of IL-10 and TNF-α, while corticosterone remained unchanged. Leptin and insulin decreased in female separates. These results suggest that ELS can induce systemic imune and metabolic alterations.