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Psychoneuroendocrinology 2019-Jun

Maternal high fat high sugar diet disrupts olfactory behavior but not mucosa sensitivity in the offspring.

Straipsnius versti gali tik registruoti vartotojai
Prisijungti Registracija
Nuoroda įrašoma į mainų sritį
Laëtitia Merle
Ophélie Person
Pierre Bonnet
Stéphane Grégoire
Vanessa Soubeyre
Xavier Grosmaitre
David Jarriault

Raktažodžiai

Santrauka

The influence of maternal diet on progeny's metabolic health has been thoroughly investigated, but the impact on sensory systems remains unexplored. Neurons of the olfactory system start to develop during the embryonic life and carry on their maturation after birth. Besides, these neurons are under metabolic influences, and it has recently been shown that adult mice exposed to an obesogenic or diabetogenic diet display reduced olfactory abilities. However, whether or not Folfactory function is affected by the perinatal nutritional environment is unknown. Here we investigated the effect of a high fat high sucrose (HFHS) maternal diet (46% of total energy brought by lipids, 26.6% by sucrose) on progeny's olfactory system in mice. In male offspring at weaning stage, maternal HFHS diet induced overweight and increased gonadal fat, associated with hyperleptinemia. The progeny of HFHS diet fed dams showed reduced sniffing behavior in the presence of low doses of phenylethanol (an attractive odorant for mice), compared to the progeny of standard diet fed dams. Furthermore, they exhibited increased time to retrieve a piece of breakfast cereals hidden beneath the bedding in a buried food test. Meanwhile, electroolfactogram recordings revealed no change in the sensitivity of olfactory mucosa. mRNA levels for elements of the olfactory transduction cascade were not affected either. Our results demonstrate that maternal HFHS diet during gestation and lactation strongly modulates olfactory perception in the offspring, without impairing odor detection by the olfactory epithelium. Maternal HFHS diet starting two months before gestation did not induce additional impairments in progeny.

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