High Salt Elicits Brain Inflammation and Cognitive Dysfunction, Accompanied by Alternations in the Gut Microbiota and Decreased SCFA Production

Hu, Li; Zhu, Shirley; Peng, Xiaoping; Li, Kanglan; Peng, Wanjuan; Zhong, Yu; Kang, Chenyao; Cao, Xingxing; Liu, Zhou; Zhao, Bin

doi:10.3233/jad-200035

Cited by 51 publications

(42 citation statements)

References 49 publications

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“…For example, how do diet-induced alterations in gut bacteria impact the brain? Several possible mechanisms have been investigated and proposed, such as impaired gut barrier function and endotoxemia 63,73 , perhaps related to altered short-chain fatty acid production 66,74 . Moreover, it is well-known that the liver is negatively impacted by excessive fructose consumption 75 , and emerging evidence highlights a gut microbiome-liver axis with crosstalk via bile acids and cytokines 76 .…”

Section: Discussionmentioning

confidence: 99%

Gut microbial taxa elevated by dietary sugar disrupt memory function

et al. 2021

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Emerging evidence highlights a critical relationship between gut microbiota and neurocognitive development. Excessive consumption of sugar and other unhealthy dietary factors during early life developmental periods yields changes in the gut microbiome as well as neurocognitive impairments. However, it is unclear whether these two outcomes are functionally connected. Here we explore whether excessive early life consumption of added sugars negatively impacts memory function via the gut microbiome. Rats were given free access to a sugar-sweetened beverage (SSB) during the adolescent stage of development. Memory function and anxiety-like behavior were assessed during adulthood and gut bacterial and brain transcriptome analyses were conducted. Taxa-specific microbial enrichment experiments examined the functional relationship between sugar-induced microbiome changes and neurocognitive and brain transcriptome outcomes. Chronic early life sugar consumption impaired adult hippocampal-dependent memory function without affecting body weight or anxiety-like behavior. Adolescent SSB consumption during adolescence also altered the gut microbiome, including elevated abundance of two species in the genus Parabacteroides (P. distasonis and P. johnsonii) that were negatively correlated with hippocampal function. Transferred enrichment of these specific bacterial taxa in adolescent rats impaired hippocampal-dependent memory during adulthood. Hippocampus transcriptome analyses revealed that early life sugar consumption altered gene expression in intracellular kinase and synaptic neurotransmitter signaling pathways, whereas Parabacteroides microbial enrichment altered gene expression in pathways associated with metabolic function, neurodegenerative disease, and dopaminergic signaling. Collectively these results identify a role for microbiota “dysbiosis” in mediating the detrimental effects of early life unhealthy dietary factors on hippocampal-dependent memory function.

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Section: Discussionmentioning

confidence: 99%

Gut microbial taxa elevated by dietary sugar disrupt memory function

et al. 2021

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“…Importantly, Th17 activation also contributes to obesity‐associated inflammation and type 2 diabetes (42). NaCL diet has also been found to induce changes in fecal short chain fatty acids (SCFAs) (43,44). SCFAs can alter host metabolism, and total levels of SCFAs correlate with insulin sensitivity; therefore, sodium‐induced changes could have important implications in both glucose control and obesity.…”

Section: Discussionmentioning

confidence: 99%

High‐fat and high‐sodium diet induces metabolic dysfunction in the absence of obesity

Frieler

Vigil

Song

et al. 2021

Obesity

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Objective Excess dietary fat and sodium (NaCl) are both associated with obesity and metabolic dysfunction. In mice, high NaCl has been shown to block high‐fat (HF) diet–induced weight gain. Here, the impact of an HF/NaCl diet on metabolic function in the absence of obesity was investigated. Methods Wild‐type mice were administered chow, NaCl (4%), HF, and HF/NaCl diets. Metabolic analysis was performed by measuring fasted blood glucose and insulin levels and by glucose tolerance test and insulin tolerance test. Results After 10 weeks on diets, male and female mice on the HF diet gained weight, and HF/NaCl mice had significantly reduced weight gain similar to chow‐fed mice. In the absence of obesity, HF/NaCl mice had significantly elevated fasting blood glucose and impaired glucose control during glucose tolerance tests. Both NaCl and HF/NaCl mice had decreased pancreas and β‐cell mass. Administration of NaCl in drinking water did not protect mice from HF‐diet‐induced weight gain and obesity. Further analysis revealed that longer administration of HF/NaCl diets for 20 weeks resulted in significant weight gain and insulin resistance. Conclusions The data demonstrate that despite early inhibitory effects on fat deposition and weight gain, an HF/NaCl diet does not prevent the metabolic consequences of HF diet consumption.

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“…For example, how do diet-induced alterations in gut bacteria impact the brain? Several possible mechanisms have been investigated and proposed, such as impaired gut barrier function and endotoxemia 64,74 , perhaps related to altered short chain fatty acid production 67,75 . Moreover it is well known that the liver is negatively impacted by excessive fructose consumption 76 , and emerging evidence highlights a gut microbiome-liver axis with crosstalk via bile acids and cytokines 77 .…”

Section: Discussionmentioning

confidence: 99%

Gut microbial taxa elevated by dietary sugar disrupt memory function

Noble¹,

Olson

Davis

et al. 2020

Preprint

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brain, microbiota, early-life, development, learning and memory 24 mediating the negative effects of early life unhealthy dietary factors on neurocognitive 48 outcomes. 49 50The gut microbiome is increasingly implicated in modulating neurocognitive 53 development and consequent functioning 1,2 . Early life developmental periods represent 54 critical windows for the impact of indigenous gut microbes on the brain, as evidenced by 55 the reversal of behavioral and neurochemical abnormalities in germ free rodents when 56 inoculated with conventional microbiota during early life, but not during adulthood [3][4][5] . 57Dietary factors are a critical determinant of gut microbiota diversity and can alter gut 58 bacterial communities, as evident from the microbial plasticity observed in response to 59 pre-and probiotic treatment, as well as the "dysbiosis" resulting from consuming 60unhealthy, yet palatable foods that are associated with obesity and metabolic disorders 61 (e.g., "Western diet"; foods high in saturated fatty acids and added sugar) 6 . In addition 62 to altering the gut microbiota, consumption of these dietary factors yields long-lasting 63 memory impairments, and these effects are more pronounced when consumed during 64 early life developmental periods vs. during adulthood 7-9 . Whether diet-induced changes 65 in specific bacterial populations are functionally related to altered early life 66 neurocognitive outcomes, however, is poorly understood. 67 68The hippocampus, which is well known for its role in spatial and episodic memory and 69 more recently for regulating learned and social aspects of food intake control 10-15 , is 70 particularly vulnerable to the deleterious effects of Western dietary factors [16][17][18] . During 71 the juvenile and adolescent stages of development, a time when the brain is rapidly 72 developing, consumption of diets high in saturated fat and sugar 19-21 or sugar alone 22-25 73 impairs hippocampal function while in some cases preserving memory processes that do 74 5 not rely on the hippocampus. While several putative underlying mechanisms have been 75investigated, the precise biological pathways linking dietary factors to neurocognitive 76 dysfunction remain largely undetermined 9 . Here we aimed to determine whether sugar-77 induced alterations in gut microbiota during early life are causally related to 78 hippocampal-dependent memory impairments observed during adulthood. 79 80 Early-life sugar consumption impairs hippocampal-dependent memory 81 function without affecting other neurocognitive domains 82 83Results from the Novel Object in Context (NOIC) task, which measures hippocampal-84 dependent episodic contextual memory function 26 , reveal that while there were no 85 differences in total exploration time of the combined objects on days 1 or 3 of the task 86 ( Fig. 1A,B), animals fed sugar solutions in early life beginning at PN 28 had a reduced 87 capacity to discriminate an object that was novel to a specific context when animals 88 were tested during adulthood (PN 6...

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High Salt Elicits Brain Inflammation and Cognitive Dysfunction, Accompanied by Alternations in the Gut Microbiota and Decreased SCFA Production

Cited by 51 publications

References 49 publications

Gut microbial taxa elevated by dietary sugar disrupt memory function

Gut microbial taxa elevated by dietary sugar disrupt memory function

High‐fat and high‐sodium diet induces metabolic dysfunction in the absence of obesity

Gut microbial taxa elevated by dietary sugar disrupt memory function

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