Juvenile exposure to a high fat diet promotes behavioral and limbic alterations in the absence of obesity

A high fat diet-induced decrease in hippocampal newly-born neurons of male mice is exacerbated by mild psychological stress using a Communication Box

“…Our results indicate that hippocampal newly-born neurons were decreased in the high fat diet-fed mice compared to the control diet-fed mice, which is consistent with the previous findings reported by several studies (Boitard et al, 2012;Gault et al, 2015;Hamilton et al, 2011;Hwang et al, 2008;Klein et al, 2016;Park et al, 2010;Pathak et al, 2015;Rivera et al, 2013;Vinuesa et al, 2016;Yoo et al, 2011aYoo et al, , 2011bYoo et al, , c, d, 2012Yoo et al, , 2014. In addition, our results indicate that psychological stress using a Communication Box caused a significant decrease in the DCX-positive neuroblasts/immature neurons in the hippocampus of the high fat diet-, but not in the control diet-fed mice.…”

“…This discrepancy may be attributed to differences in the experimental protocols, including the content of the fat diet, the duration of feeding, and the mouse strain. Of note, in the previous study, the high fat diet-fed mice did not become obese because of the moderate high fat diet provided (Vinuesa et al, 2016).…”

“…Sharma and Fulton (2013) reported that high fat diet-induced obese mice exhibit a negative emotional state and hyperactivity of the stress response, which may be involved in the high fat diet-induced decrease in the ventral hippocampal neurogenesis observed in the present study. Although little has been reported on the impacts of high fat dietinduced obesity on hippocampal neurogenesis of the dorsal and ventral DG separately, a study by Vinuesa et al (2016) indicated that 4-months of feeding a 20% high fat diet to C57BL/6J mice resulted in a decrease in hippocampal neurogenesis in the dorsal part of the DG, but not the ventral part. This discrepancy may be attributed to differences in the experimental protocols, including the content of the fat diet, the duration of feeding, and the mouse strain.…”

“…We previously found that hippocampal neurogenesis is increased by chronic administration of tandospirone, a clinically available 5-HT1A receptor partial agonist with anxiolytic and antidepressant effects, under stress and non-stress conditions (Mori et al, 2014;Murata et al, 2015). Many researchers have reported that neurogenesis in the hippocampal DG is decreased in rodents with a chronic intake of obesogenic diets, including a high fat diet (Boitard et al, 2012;Gault et al, 2015;Hamilton et al, 2011;Hwang et al, 2008;Klein et al, 2016;Park et al, 2010;Pathak et al, 2015;Rivera et al, 2013;Vinuesa et al, 2016;Yoo et al, 2011aYoo et al, , b, c, d, 2012Yoo et al, , 2014. Of interest, recent data demonstrate that a decrease in hippocampal neurogenesis contributes to the dysregulation of the hypothalamuspituitary-adrenal (HPA) axis and the activation of a stress response (Dranovsky and Leonardo, 2012;Snyder et al, 2011).…”

High-Fat-Diet-Induced Deficits in Dopamine Terminal Function Are Reversed by Restoring Insulin Signaling

“…1–3 An emerging body of evidence has revealed that insulin plays multiple roles in the brain, expanding on its well-known function to regulate glucose homeostasis and energy balance via the hypothalamus. 4–6 Recent studies have shown that insulin modulates dopamine neurotransmission by altering the excitability of dopamine neuron cell bodies in the ventral tegmental area (VTA), 7–9 in addition to augmenting dopamine release in striatal terminal fields.…”