To read the full abstract: Psychoneuroendocrinology. 2018 Dec 6;102:128138.
This study investigated whether maternal high fat diet (HFD) exposure during rat pregnancy and lactation can alter the hypothalamic-pituitary-adrenal (HPA) in adult male offspring.
Maternal diet and metabolic status are important factors which influence the intrauterine and early postnatal environment that offspring experiences in early life. There is accumulating evidence supporting that perinatal overnutrition or high fat HFD consumption may result in developmental and health problems, such as metabolic syndrome, hypertension, cardiovascular remodeling and cerebrovascular dysfunction. Moreover, maternal HFD exposure also confers offspring susceptibility to behavioral disorders and mental problems, including anxiety, depression, cognitive deficit, impairments in social behavior and reward-based behaviors. As the core mediator of the neuroendocrine stress response, HPA axis is subject to programming by early life challenges.
This study provides further evidence for the long-lasting influence of maternal diet exposure on the development of the HPA axis in adult offspring. The experiments support the hypothesis that a fat rich diet during pregnancy and lactation fundamentally alters the activity of the HPA axis in adult offspring, under both stress-free and stressful conditions. The maternal HFD-induced remodeling of the HPA axis would ultimately not only affect the adult responsiveness to the stressful challenge, but also give rise to an offspring phenotype predisposed to the development of behavior disorders and other health problems in adult. The present study demonstrated, for the first time that a maternal diet affects the HPA response in a stressor-specific manner, with alternations of the neuroendocrine response to psychological and systemic but not metabolic stressors.
Moreover, the medial and central regions of the amygdala play an important role in the hyperresponsiveness of the HPA axis to psychological and systemic stress in maternal HFD offspring, respectively, suggesting that maternal HFD exposure may selectively modulate the HPA response to different incoming signals through differential neural pathways. Identification of the mechanisms and pathways that produce long-term vulnerability in response to perinatal environmental factors will facilitate development of clinical intervention and prevention strategies to reduce the incidence and severity of disease. Therefore, more studies need to be conducted to characterize the pathways and mechanisms by which maternal HFD consumption influences the HPA axis activity.