Abstract
Maternal hypercaloric exposure during pregnancy and lactation is a risk factor for developing diseases associated with inflammation such as obesity, diabetes and, neurological diseases in the offspring. Neuroinflammation might modulate neuronal activation and flavonoids are dietary compounds that have been proven to exert anti-inflammatory properties. Thus, the aim of the present study is to evaluate the effect of maternal supplementation with flavonoids (kaempferol-3-O-glucoside and narirutin) on the prevention of depression-like behaviour in the female offspring of dams fed with an obesogenic diet during the perinatal period. Maternal programming was induced by high fat (HFD), high sugar (HSD), or cafeteria diets exposure and depressive like-behaviour, referred to as swimming, climbing, and immobility events, was evaluated around postnatal day 56–60 before and after 30 mg/kg i.p. imipramine administration in the female offspring groups. Central inflammation was analyzed by measuring the TANK binding kinase 1 (TBK1) expression. We found that the offspring of mothers exposed to HSD programming failed to show the expected antidepressant effect of imipramine. Also, imipramine injection, to the offspring of mothers exposed to cafeteria diet, displayed a pro-depressive like-behaviour phenotype. However, dietary supplementation with flavonoids reverted the depression-like behaviour in the female offspring. Finally, we found that HSD programming increases the TBK1 inflammatory protein marker in the hippocampus. Our data suggest that maternal HSD programming disrupts the antidepressant effect of imipramine whereas cafeteria diet exposure leads to depressive-like behaviour in female offspring, which is reverted by maternal flavonoid supplementation.
Highlights
Depression affects more than 300 million people worldwide and is one of the leading causes of disability (World Health Organization)
We found that found that cafeteria diet exposure programs female offspring to be unresponsive to the anticafeteria diet exposure programs female offspring to be unresponsive to the anti-depressive effect of imipramine, showing no changes in swimming, climbing, and immobility counts when compared to the cafeteria group (Figure 4B–D)
These results suggest that in contrast to nutritional programming by high fat diet (HFD) exposure, high sugar diet (HSD) seems to disrupt the sensitivity to pharmacologic inhibition of depression and that flavonoids recover the anti-depressive effect of imipramine in offspring linked to cafeteria nutritional programming
Summary
Depression affects more than 300 million people worldwide and is one of the leading causes of disability (World Health Organization). Maternal programming by hypercaloric diet exposure sets a peripheral and central inflammation which modulates defective behaviour in the offspring, favoring depression-like behaviour phenotypes in murine models [10,11,12,13,14]. Central TLR4 activation by saturated fatty acids leads to inflammatory response and metabolic complications [17,18]. Hypercaloric programming during pregnancy sets a peripheral and central inflammatory profile leading to metabolic complications and depression susceptibility in offspring
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