Olive oil-rich diet during pregnancy/lactation attenuated the early life stress effects on depressive-like behavior and altered energy metabolism in the dorsal hippocampus in a sex-specific manner

NUTRITIONAL NEUROSCIENCE(2022)

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摘要
Scope: Maternal separation (MS), may cause depressive-like behavior in adulthood energy metabolism dysfunction appears to be a key factor in this pathophysiology. Olive oil (OO) consumption may be a strategy for improving energy metabolism. Our aim was to investigate if a maternal OO-enrich diet during pregnancy/lactation could attenuate MS effects on depressive-like behavior and energy metabolism in the dorsal hippocampus (DH) of adult male and female rats. Methods and results: Pregnant Wistar rats received diets enriched in soybean oil (SO) or OO during gestation/lactation. At birth, litters were subdivided into MS or intact groups. After weaning, the pups received standard chow until adulthood, when they were subjected to behavioral tasks. At PND90 biochemical analyses were performed. Maternal OO-enriched diet prevented MS-induced higher weight gain, and decreased MS-induced anhedonic behavior. Increased latency to immobility and shorter immobility time were observed in the maternal OO-enrich diet groups. Maternal OO-enrich diet groups also presented reduced reactive oxygen species and increased activity of antioxidant enzymes. In addition, this diet showed sex-specific effects, by decreasing mitochondrial mass and potential, reducing AMPK activation, and increasing synaptophysin and PSD-95 immunocontent in the DH of male rats. Early stress, on the other hand, decreased production of free radicals and decreased levels of SIRT1 in the DH of male rats. In females, OO prevented the anhedonic behavior induced by MS. Conclusions: Maternal OO-enrich diet attenuated MS-induced depressive behavior in both sexes. In addition, it affected energy metabolism in the DH of male rats, favored synaptic plasticity, and contributed to reducing pathophysiological conditions.
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Olive oil, maternal separation&#8204, depression, mitochondria, AMPK, SIRT-1, oxidative stress, sex-specific
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