The effect of short-term exposure to energy-matched diets enriched in fat or sugar on memory, gut microbiota and markers of brain inflammation and plasticity

Beilharz, Jessica E.; Kaakoush, Nadeem O.; Maniam, Jayanthi; Morris, Margaret J.

doi:10.1016/j.bbi.2016.07.151

Cited by 80 publications

(56 citation statements)

References 45 publications

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“…However as previously described [13, 65, 66] after this first phase, the animals were able to control their energy intake. Changes in microbiota composition have been shown to be very dynamic and detectable as early as 1 to 2 weeks following changes in diet composition [68, 69] with some studies suggesting that a single meal could trigger compositional changes and increase endotoxemia [70, 71]. Therefore, it appears unlikely that the initial hyperphagia would have a lasting influence on the microbiota composition at week 4.…”

Section: Resultsmentioning

confidence: 99%

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Sen

Cawthon

Ihde

et al. 2017

Physiology & Behavior

200

152

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Obesity is one of the major health issues in the United States. Consumption of diets rich in energy, notably from fats and sugars (high-fat/high-sugar diet: HF/HSD) is linked to the development of obesity and a popular dietary approach for weight loss is to reduce fat intake. Obesity research traditionally uses low and high fat diets and there has been limited investigation of the potential detrimental effects of a low-fat/high-sugar diet (LF/HSD) on body fat accumulation and health. Therefore, in the present study, we investigated the effects of HF/HSD and LF/HSD on microbiota composition, gut inflammation, gut-brain vagal communication and body fat accumulation. Specifically, we tested the hypothesis that LF/HSD changes the gut microbiota, induces gut inflammation and alters vagal gut-brain communication, associated with increased body fat accumulation. Sprague-Dawley rats were fed an HF/HSD, LF/HSD or control low-fat/low-sugar diet (LF/LSD) for 4 weeks. Body weight, caloric intake, and body composition were monitored daily and fecal samples were collected at baseline, 1, 6 and 27 days after the dietary switch. After four weeks, blood and tissues (gut, brain, liver and nodose ganglia) were sampled. Both HF/HSD and LF/HSD-fed rats displayed significant increases in body weight and body fat compared to LF/LSD-fed rats. 16S rRNA sequencing showed that both HF/HSD and LF/HSD-fed animals exhibited gut microbiota dysbiosis characterized by an overall decrease in bacterial diversity and an increase in Firmicutes/Bacteriodetes ratio. Dysbiosis was typified by a bloom in Clostridia and Bacilli and a marked decrease in Lactobacillus spp. LF/HSD-fed animals showed a specific increase in Sutterella and Bilophila, both Proteobacteria, abundances of which have been associated with liver damage. Expression of pro-inflammatory cytokines, such as IL-6, IL-1β and TNFα was upregulated in the cecum while levels of tight junction protein occludin were downregulated in both HF/HSD and LF/HSD fed rats. HF/HSD and LF/HSD-fed rats also exhibited an increase in cecum and serum levels of lipopolysaccharide (LPS), a pro-inflammatory bacterial product. Immunofluorescence revealed the withdrawal of vagal afferents from the gut and at their site of termination the nucleus of the solitary tract (NTS) in both the HF/HSD and LF/HSD rats. Moreover, there was significant microglia activation in the nodose ganglia, which contain the vagal afferent neuron cell bodies, of HF/HSD and LF/HSD rats. Taken together, these data indicate that, similar to HF/HSD, consumption of an LF/HSD induces dysbiosis of gut microbiota, increases gut inflammation and alters vagal gut-brain communication. These changes are associated with an increase in body fat accumulation.

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Section: Resultsmentioning

confidence: 99%

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Sen

Cawthon

Ihde

et al. 2017

Physiology & Behavior

200

152

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“…Ruminococcaceae have shown a range of macronutrient-specific negative correlations with place memory 42 ; thus, this phylum plays an important role in cognitive function. In our results, the abundance of the genera Ruminiclostridium_9 and Ruminococcaceae_UCG_010, both of which belong to the family Ruminococcaceae, was much higher in the METH CPP group than in the control group.…”

Section: Discussionmentioning

confidence: 99%

Gut microbiota analysis in rats with methamphetamine-induced conditioned place preference

Ning

Gong

Xie

et al. 2017

Preprint

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Methamphetamine abuse is a major public health crisis. Because accumulating evidence supports the hypothesis that the gut microbiota plays an important role in central nervous system (CNS) function, and research on the roles of the microbiome in CNS disorders holds conceivable promise for developing novel therapeutic avenues for treating CNS disorders, we sought to determine whether administration of methamphetamine leads to alterations in the intestinal microbiota. In this study, the gut microbiota profiles of rats with methamphetamineinduced conditioned place preference (CPP) were analysed through 16S rRNA gene sequencing.The faecal microbial diversity was slightly higher in the METH CPP group. The propionateproducing genus Phascolarctobacterium was attenuated in the METH CPP group, and the family Ruminococcaceae was elevated in the METH CPP group. Short chain fatty acid analysis revealed that the concentrations of propionate were decreased in the faecal matter of METHadministered rats. These findings provide direct evidence that administration of METH causes gut dysbiosis, enable a better understanding of the function of gut microbiota in the process of drug abuse, and provide a new paradigm for addiction treatment.

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“…While it is known that excessive consumption of diets high in saturated fat and sugar is associated with cognitive impairment [1][2][3] and increased risk of neurodegenerative disease 4,5 , the underlying causative mechanisms remain controversial. Substantial evidence indicates that such diets are associated with low-grade systemic 6,7 and central 8 inflammation, and diet-induced hippocampal proinflammatory changes are associated with impaired performance on hippocampal-dependent cognitive tasks in rats [9][10][11][12][13] and mice [14][15][16] . However, other mechanisms, such as increased oxidative stress 13 , reduced sirtuin expression 12 and neurotrophic factors 15,17,18 , and altered synaptic plasticity 19 have also been implicated in dietinduced cognitive impairment.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, minocycline has antibiotic activity and has been recently reported to reduce some effects of high-fat diet in rats through altering food intake and the gut microbiome composition 27 . Given the role of the gut microbiome in diet-induced cognitive impairment 11,28,29 , it is important to examine the effects of minocycline on microbiome composition and to investigate potential behavioral associations as these have not been previously studied.…”

Section: Introductionmentioning

confidence: 99%

Minocycline-induced microbiome alterations predict cafeteria diet-induced spatial recognition memory impairments in rats

et al. 2020

Self Cite

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Diets rich in sugar and saturated fat are associated with cognitive impairments in both humans and rodents with several potential mechanisms proposed. To test the involvement of diet-induced pro-inflammatory signaling, we exposed rats to a high-fat, high-sugar cafeteria diet, and administered the anti-inflammatory antibiotic minocycline. In the first experiment minocycline was coadministered across the diet, then in a second, independent cohort it was introduced following 4 weeks of cafeteria diet. Cafeteria diet impaired novel place recognition memory throughout the study. Minocycline not only prevented impairment in spatial recognition memory but also reversed impairment established in rats following 4 weeks cafeteria diet. Further, minocycline normalized diet-induced increases in hippocampal pro-inflammatory gene expression. No effects of minocycline were seen on adiposity or dietary intake across the experiments. Cafeteria diet and minocycline treatment significantly altered microbiome composition. The relative abundance of Desulfovibrio_OTU31, uniquely enriched in vehicle-treated cafeteria-fed rats, negatively and significantly correlated with spatial recognition memory. We developed a statistical model that accurately predicts spatial recognition memory based on Desulfovibrio_OTU31 relative abundance and fat mass. Thus, our results show that minocycline prevents and reverses a dietary-induced diet impairment in spatial recognition memory, and that spatial recognition performance is best predicted by changes in body composition and Desulfovibrio_OTU31, rather than changes in pro-inflammatory gene expression.

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The effect of short-term exposure to energy-matched diets enriched in fat or sugar on memory, gut microbiota and markers of brain inflammation and plasticity

Cited by 80 publications

References 45 publications

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity

Gut microbiota analysis in rats with methamphetamine-induced conditioned place preference

Minocycline-induced microbiome alterations predict cafeteria diet-induced spatial recognition memory impairments in rats

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