Cafeteria-diet effects on cognitive functions, anxiety, fear response and neurogenesis in the juvenile rat

Ferreira, André; Castro, João Paulo; Andrade, José Paulo; Madeira, M. Dulce; Cardoso, Armando

doi:10.1016/j.nlm.2018.07.014

Cited by 45 publications

(46 citation statements)

References 81 publications

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“…Despite a wide range of use in rodent models of obesity, purified high fat diets do not reflect a true Westernized diet and therefore may exert an insufficient response in obesity development occasionally (Oliva et al, 2017). For this reason, cafeteria diets are considered to be a more efficient diet induced obesity model, comparatively as they introduce a variety of highly palatable energy dense foods that are widely consumed in Western societies (Ferreira et al, 2018). As reported before in previous studies, current study also exhibited that not all high fat diets induced obesity in young rats while cafeteria diet provided a highly relevant diet induced obesity model in terms of reflecting a human diet.…”

Section: Discussionmentioning

confidence: 99%

Cafeteria diet increased adiposity in comparison to high fat diet in young male rats

Büyükdere

Güleç

Akyol

2019

PeerJ

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Background Dietary intervention studies in animal models of obesity are crucial to elucidate the mechanistic effects of specific nutrients and diets. Although several models of diet induced obesity have been examined in rodents to assess obesity, there are few studies that have researched influence of different high fat and/or westernized diets. The aim of this study was to compare a high fat diet and a cafeteria diet on obesity related biochemical and physiological parameters in young male rats. Methods Five week old Wistar male rats were fed a control chow diet (C), butter-based high fat diet (HF) or cafeteria diet (CAF) for twelve weeks. In HF, 40% of energy came from fat and this ratio was 46% in CAF. CAF composed of highly energetic and palatable human foods along with chow diet. At the end of the feeding protocol all animals were culled using CO2 asphyxia and cervical dislocation after an overnight fasting. Results Total energy and fat intake of CAF was significantly higher than C and HF. CAF was more effective in inducing obesity, as demonstrated by increased weight gain, Lee index, fat depot weights and total body fat in comparison to C and HF. Despite increased adiposity in CAF, plasma glucose, insulin and HOMA-IR levels were similar between the groups. Plasma leptin and cholesterol levels were markedly higher in CAF than C and HF. Discussion We have demonstrated that there are differential effects of high fat diet and cafeteria diet upon obesity and obesity-related parameters, with CAF leading to a more pronounced adiposity in comparison to high fat diet in young male rats. Future studies should consider the varied outcomes of different diet induced obesity models and development of a standardized approach in similar research practices.

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Section: Discussionmentioning

confidence: 99%

Cafeteria diet increased adiposity in comparison to high fat diet in young male rats

Büyükdere

Güleç

Akyol

2019

PeerJ

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“…Such findings may help to explain neuroimaging data showing brain atrophy, including reduced hippocampal gray matter, among rats fed a HFD in adolescence or young adulthood (Kalyan-Masih et al, 2016; Rollins et al, 2019). Adolescent sucrose access has been associated with reductions in neurogenesis or neuroproliferation in some (Gueye et al, 2018) but not all studies (Ferreira et al, 2018; Xu and Reichelt, 2018). Sucrose exposure during this developmental period has also been shown to result in reductions in hippocampal parvalbumin-containing ⋎-aminobutyric acid (GABA)-ergic interneurons, thought to be critical for memory processes (Fuchs et al, 2007; Ognjanovski et al, 2017) and implicated in Alzheimer's disease pathology (Zallo et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Examining Adolescence as a Sensitive Period for High-Fat, High-Sugar Diet Exposure: A Systematic Review of the Animal Literature

Murray

Chen

2019

Front. Neurosci.

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Animal studies suggest that poor nutrition (e.g., high-fat, high-sugar diets) may lead to impairments in cognitive functioning. Accumulating evidence suggests that the deleterious effects of these diets appear more pronounced in animals maintained on this diet early in life, consistent with the notion that the developing brain may be especially vulnerable to environmental insults. The current paper provides the first systematic review of studies comparing the effects of high-fat, high-sugar diet exposure during adolescence and adulthood on memory performance. The majority of studies (7/8) identified here report diet-induced memory problems when diet exposure began in adolescence but not adulthood. These findings lend support to the hypothesis that adolescence is a sensitive period during which palatable diets may contribute to negative neurocognitive effects. The current review explores putative mechanisms involved in diet-induced cognitive dysfunction and highlights promising areas for further research.

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“…We and others have used rodent models to show that a western-style cafeteria diet, high in fat and sugar, promotes prolonged hyperphagia and increases adiposity, compromising metabolic health [4][5][6] . Exposure to such diets impairs performance on hippocampal-dependent tasks assessing short-term spatial recognition 2,7 and reference 8,9 memory, as well as disrupting multiple hippocampal molecular pathways, including pro-inflammatory signaling 7,8,10 , blood-brain barrier integrity 3,11 and synaptic transmission 12 , and inducing fecal microbiome perturbations 13,14 . However, no one of these physiological changes has been consistently tied to the behavioral phenotype and limited studies targeting causation have been undertaken.…”

Section: Introductionmentioning

confidence: 99%

Intermittent cafeteria diet identifies fecal microbiome changes as a predictor of spatial recognition memory impairment in female rats

et al. 2020

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Excessive consumption of diets high in saturated fat and sugar impairs short-term spatial recognition memory in both humans and rodents. Several studies have identified associations between the observed behavioral phenotype and diet-induced changes in adiposity, hippocampal gene expression of inflammatory and blood-brain barrier-related markers, and gut microbiome composition. However, the causal role of such variables in producing cognitive impairments remains unclear. As intermittent cafeteria diet access produces an intermediate phenotype, we contrasted continuous and intermittent diet access to identify specific changes in hippocampal gene expression and microbial species that underlie the cognitive impairment observed in rats fed continuous cafeteria diet. Female adult rats were fed either regular chow, continuous cafeteria diet, or intermittent cafeteria diet cycles (4 days regular chow and 3 days cafeteria) for 7 weeks (12 rats per group). Any cafeteria diet exposure affected metabolic health, hippocampal gene expression, and gut microbiota, but only continuous access impaired short-term spatial recognition memory. Multiple regression identified an operational taxonomic unit, from species Muribaculum intestinale, as a significant predictor of performance in the novel place recognition task. Thus, contrasting intermittent and continuous cafeteria diet exposure allowed us to identify specific changes in microbial species abundance and growth as potential underlying mechanisms relevant to diet-induced cognitive impairment.

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Cafeteria-diet effects on cognitive functions, anxiety, fear response and neurogenesis in the juvenile rat

Cited by 45 publications

References 81 publications

Cafeteria diet increased adiposity in comparison to high fat diet in young male rats

Cafeteria diet increased adiposity in comparison to high fat diet in young male rats

Examining Adolescence as a Sensitive Period for High-Fat, High-Sugar Diet Exposure: A Systematic Review of the Animal Literature

Intermittent cafeteria diet identifies fecal microbiome changes as a predictor of spatial recognition memory impairment in female rats

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