Abstract
The negative impact of obesity on neurocognitive functioning is an issue of increasing clinical interest. Over the last decade, a number of studies have analyzed the influence of high-fat diets (HFDs) on cognitive performance, particularly in adolescent individuals. Different approaches, including behavioral, neurochemical, electrophysiological and morphological studies, have been developed to address the effect of HFDs on neural processes interfering with learning and memory skills in rodents. Many of the studies have focused on learning and memory related to the hippocampus and the mechanisms underlying these processes. The goal of the current review article is to highlight the relationship between hippocampal learning/memory deficits and nutritional/endocrine inputs derived from HFDs consumption, with a special emphasis on research showing the effect of HFDs intake during the juvenile period. We have also reviewed recent research regarding the effect of HFDs on hippocampal neurotransmission. An overview of research suggesting the involvement of fatty acid (FA) receptor-mediated signaling pathways in memory deficits triggered by HFDs is also provided. Finally, the role of leptin and HFD-evoked hyperleptinemia is discussed.
Highlights
Elevated consumption of so-called western diets (WDs) is one of the main causes of overweight and obesity and a matter of concern for public health institutions
The negative impact of High-fat diet (HFD) on hippocampal neurogenesis has been the focus of many studies (Hwang et al, 2008; Park et al, 2010), some of which have shown a differential effect on animals that started to consume a HFD after weaning compared to those that consumed the diet during adulthood (Boitard et al, 2012)
A study carried out in obese mice that consumed HFD during the adolescent period, has shown that HFD improves glutamate (GLU) up-take kinetics along with the up-regulation of glial GLU transporters (GLT-1 and GLAST) and a concomitant down-regulation of glutamine synthase. This treatment led to the down-regulation of the glucose transporter GLUT-1 (Valladolid-Acebes et al, 2012). All of these findings suggest that HFD can trigger a dramatic de-regulation of GLU turnover and provides further support for the above-mentioned changes in hippocampus synaptic transmission and plasticity elicited by HFD interventions during the juvenile period
Summary
Elevated consumption of so-called western diets (WDs) is one of the main causes of overweight and obesity and a matter of concern for public health institutions. The damaging effect of these diets seems to be related to their content in terms of both saturated fat and assimilated carbohydrates, and to the fact that they promote disorganized feeding patterns consisting of frequent energy-dense snacking and/or copious meals before bedtime (Corwin and Hajnal, 2005; Matheson et al, 2012, 2014). The concept and term ‘‘comfort food’’ has been coined, referring to the consumption of palatable, high caloric food to mitigate stress and/or anxiety (Dallman et al, 2003)
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