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Obesity, anxiety, stress coping behaviors, mice
Abstract:
Background: There is growing evidence that maternal obesity and prenatal
exposure to a high-fat diet program fetal development to regulate the
physiology and behavior of the offspring in adulthood. Yet the extent to
which the maternal dietary environment contributes to adult disease
vulnerability remains unclear. In the current study we tested whether
prenatal exposure to maternal obesity increases the offspring's
vulnerability to stress-related psychiatric disorders. Methods: We used
a mouse model of maternal diet-induced obesity to investigate whether
maternal obesity affects the response to adult chronic stress exposure
in young adult (3-month-old) and aged adult (12-month-old) offspring.
Results: Long-lasting, delayed impairments to anxiety-like behaviors and
stress coping strategies resulted on account of prenatal exposure to
maternal obesity. Although maternal obesity did not change the
offspring's behavioral response to chronic stress per se, we demonstrate
that the behavioral outcomes induced by prenatal exposure to maternal
obesity parallel the deleterious effects of adult chronic stress
exposure in aged male mice. We found that the glucocorticoid receptor
(GR, Nr3c1) is upregulated in various hypothalamic nuclei on account of
maternal obesity. In addition, gene expression of a known regulator of
the GR, FKBP51, is increased specifically within the paraventricular
nucleus. Conclusions: These findings indicate that maternal obesity
parallels the deleterious effects of adult chronic stress exposure, and
furthermore identifies GR/FKBP51 signaling as a novel candidate pathway
regulated by maternal obesity. (C) 2015 S. Karger AG, Basel
