Prenatal Food Restriction Induces a Hypothalamic-Pituitary-Adrenocortical Axis-associated Neuroendocrine Metabolic Programmed Alteration in Adult Offspring Rats

Background and Aims terine growth restriction produces susceptibility to adult metabolic syndrome, which may be caused by the permanent alteration of the hypothalamic-pituitary-adrenocortical (HPA) axis. We aimed to verify that HPA axis-associated neuroendocrine metabolic programming is altered in food-restricted (FR) offspring. s al rats were fed a restricted diet from gestational day 11 until full-term delivery, all pups were fed a high-fat diet after weaning and exposed to unpredictable chronic stress (UCS) during postnatal weeks 17–20. s levels of adrenocorticotrophic hormone and corticosterone in adult offspring of the prenatal FR group were lower than the control (CN) rats before UCS but increased significantly after UCS. Serum glucose levels in the FR group were normal before UCS but increased after UCS. Serum insulin levels were significantly decreased in FR males but showed a slight increase in FR females before UCS; however, insulin levels decreased significantly in the FR male and female rats after UCS. Before UCS, serum lipid levels were higher in the FR males but were normal in the FR females; after UCS, FR males had a slight decrease and FR females had an increasing trend in serum lipids levels. Lipid droplets in the hypothalamus, pituitary gland, and livers of the FR group indicated steatosis. sions results suggest that prenatal food restriction alters HPA axis-associated neuroendocrine metabolism in adult offspring fed a high-fat diet, which may originate from the intrauterine programming and increase the susceptibility to adult metabolic diseases.