Maternal high-fat diet leads to hippocampal and amygdala dendritic remodeling in adult male offspring.

Yoottana Janthakhin, Marion Rincel, Anna-Maria Costa, Muriel Darnaudéry, Guillaume Ferreira
Psychoneuroendocrinology. 2017-09-01; 83: 49-57
DOI: 10.1016/j.psyneuen.2017.05.003

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Janthakhin Y(1), Rincel M(1), Costa AM(1), Darnaudéry M(2), Ferreira G(3).

Author information:
(1)INRA, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France;
Université de Bordeaux, Nutrition and Integrative Neurobiology, UMR 1286,
Bordeaux, France.
(2)INRA, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France;
Université de Bordeaux, Nutrition and Integrative Neurobiology, UMR 1286,
Bordeaux, France. Electronic address: .
(3)INRA, Nutrition and Integrative Neurobiology, UMR 1286, Bordeaux, France;
Université de Bordeaux, Nutrition and Integrative Neurobiology, UMR 1286,
Bordeaux, France. Electronic address: .

Early-life exposure to calorie-dense food, rich in fat and sugar, contributes to
the increasing prevalence of obesity and its associated adverse cognitive and
emotional outcomes at adulthood. It is thus critical to determine the impact of
such nutritional environment on neurobehavioral development. In animals, maternal
high-fat diet (HFD) consumption impairs hippocampal function in adult offspring,
but its impact on hippocampal neuronal morphology is unknown. Moreover, the
consequences of perinatal HFD exposure on the amygdala, another important
structure for emotional and cognitive processes, remain to be established. In
rats, we show that adult offspring from dams fed with HFD (45% from fat,
throughout gestation and lactation) exhibit atrophy of pyramidal neuron dendrites
in both the CA1 of the hippocampus and the basolateral amygdala (BLA). Perinatal
HFD exposure also impairs conditioned odor aversion, a task highly dependent on
BLA function, without affecting olfactory or malaise processing. Neuronal
morphology and behavioral alterations elicited by perinatal HFD are not
associated with body weight changes but with higher plasma leptin levels at
postnatal day 15 and at adulthood. Taken together, our results suggest that
perinatal HFD exposure alters hippocampal and amygdala neuronal morphology which
could participate to memory alterations at adulthood.

Copyright © 2017 Elsevier Ltd. All rights reserved.

DOI: 10.1016/j.psyneuen.2017.05.003
PMID: 28595087

Auteurs Bordeaux Neurocampus