Dietary emulsifier consumption accelerates type 1 diabetes development in NOD mice
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ABSTRACT:
PROVIDER: PRJEB67708 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12142700_1.fastq.gz | Fastqsanger.gz | |||
| ERR12142700_2.fastq.gz | Fastqsanger.gz | |||
| ERR12142800_1.fastq.gz | Fastqsanger.gz | |||
| ERR12142800_2.fastq.gz | Fastqsanger.gz | |||
| ERR12142900_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The goal of the current study was to test whether emulsifier consumption is associated with changes in gene expression in the amygdala and PVN Methods: Adult male C57BL/6J mice received drinking water containing either 1% sodium carboxymethylcellulose (CMC), 1% polysorbate-80 (P80) or water without emulsifier for 12 weeks. PVN and amygdala gene expression was generated by RNA-Seq using an Illumina NextSeq 500. FastQ quality filter was used to filter low quality sequences and Tophat, Bowtie, Cufflinks, and Cuffdiff were used for RNA-Seq analysis. qRT–PCR validation was performed using 6 differential genes of interest. Results: A total of 243 genes were differentially expressed in the amygdala and PVN of emulsifier-treated mice compared to controls. There was minimal overlap of differentially expressed genes in CMC- and P80-treated animals, suggesting that each emulsifier acts via distinct molecular mechanisms to produce an anxiety-like phenotype. Furthermore, gene ontology and pathway analysis revealed that various stress, metabolic, and immune terms and pathways were altered in emulsifier conditions. RNA-seq data was validated with qRT–PCR data (R2= 0.8815). Conclusions: These findings are the first to demonstrate that emulsifier consumption changes gene expression in brain regions that are critical for stress responding, providing possible molecular mechanisms that may underly the observed anxiety-like phenotype
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Project description:Modern lifestyle is associated with a major consumption of ultra-processed foods (UPF) due to their practicality and palatability. The ingestion of emulsifiers, a main additive in UPFs, has been related to gut inflammation, microbiota dysbiosis, adiposity and obesity. Maternal unbalanced nutritional habits during embryonic and perinatal stages perturb offspring’s long-term metabolic health, thus increasing obesity and associated comorbidity risk. However, whether maternal emulsifier consumption influences developmental programming in the offspring remains unknown. Here we show that, in mice, maternal consumption of dietary emulsifiers (1% CMC and 1% P80 in drinking water), during gestation and lactation, perturbs the development of hypothalamic energy balance regulation centers of the progeny, leads to metabolic impairments, cognition deficits and induces anxiety-like traits in a sex-specific manner. Our findings support the notion that maternal consumption of emulsifiers, common additives of UPFs, causes mild metabolic and neuropsychological malprogramming in the progeny. Our data call for nutritional advice during gestation.
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Project description:The purpose of this study was to analyze and elucidate the mechanisms of non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE), an animal model of progressive multiple sclerosis (MS), and to compare the pathological features with those observed in human progressive MS. To achieve this, pathological analysis, flow cytometry analysis, immunohistochemical staining, and transcriptome analysis were performed at each pathological stage of the NOD-EAE mice to characterize each pathological stages in the lesion. In the chronic phase of the NOD-EAE mice, fibrosis and lymph follicle formation, characteristic of progressive human MS, were observed. We describe the pathological profile and transcriptome analysis of the NOD-EAE mice and verify that this model has similar features to those of human progressive MS. Our findings suggest that this model recapitulates lymph follicle formation, a disease hallmark of progressive MS, and fibrosis, a feature complicating the pathogenesis of MS in the chronic phase.
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Project description:in vitro microbiota model recapitulates and predicts individualized sensitivity to dietary emulsifier
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Project description:We used high density oligonucleotide arrays to measure the relative expression levels of >39,000 genes and ESTs in the NOD mouse (a murine model of T1D and other autoimmune conditions), four NOD-derived diabetes resistant congenic strains and two nondiabetic control strains. Owing to the importance of T cells in the development of T1D we decided to target two organs, the spleen and thymus. We profiled gene expression in thymi from four week old female mice and spleens from three month old female mice. For each of the 14 strain-tissue combinations (7 strains x 2 tissues) we performed two independent replicate experiments, making the total number of hybridizations performed 28. In each case, an RNA population from a pool of two or three organs was generated to minimize the chances of within strain variation masking genuine variation between the strains. To minimize any variation introduced during target preparation, all samples within a given replicate group were processed in parallel. Three samples from group two (spleen: B10.H2g7_S2 http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=gsm594 (GSM594); thymus: B10.H2g7_T2 http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=gsm608 (GSM608), B10.H2g7 Idd3_T2 http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=gsm609 (GSM609)) and one from group one (spleen B10.H2g7_S1 http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=gsm587 (GSM587) failed a preliminary quality control check. Consequently, the steps involved in preparing labelled cRNA from the initial starting material had to be repeated for these four samples at a later date. A subsequent comparison of the variation seen between samples within the same replicate group (samples processed in parallel) versus samples in distinct replicate groups (samples processed at different times) revealed that the variation between the two groups (i.e. owing to independent sample preparation) was higher than the small amount of variation between the closely matched strains. Ignoring the variability introduced during sample preparation was therefore likely to result in spurious changes being detected and genuine strain-specific differences in gene expression being masked. Consequently, we decided to exclude the four samples that had had to be prepared independently owing to failing initial quality control. Keywords = NOD, diabetes, congenic Keywords: other
2001-11-21 | GSE11 | GEO
Project description:Dietary emulsifiers, including carboxymethylcellulose (CMC) and polysorbate 80 (P80), perturb gut microbiota composition and gene expression, resulting in a microbiota with enhanced capacity to activate host pro-inflammatory gene expression and invade the intestine's inner mucus layer. Such microbiota alterations promote intestinal inflammation, which can have a variety of phenotypic consequences including increased adiposity. Bacterial flagellin is a key mediator of emulsifiers' impact in that this molecule enables motility and is itself a pro-inflammatory agonist. Hence, we reasoned that training the adaptive mucosal immune system to exclude microbes that express flagellin might protect against emulsifiers. Investigating this notion found that immunizing mice with flagellin elicited an increase in mucosal anti-flagellin IgA and IgA-coated microbiota that would have otherwise developed in response to CMC and P80 consumption. Yet, eliciting these responses in advance via flagellin immunization prevented CMC/P80-induced increases in microbiota expression of pro-inflammatory agonists including LPS and flagellin. Furthermore, such immunization prevented CMC/P80-induced microbiota encroachment and deleterious pro-inflammatory consequences associated therewith, including colon shortening and increased adiposity. Hence, eliciting mucosal immune responses to pathobiont surface components, including flagellin, may be a means of combatting the array of inflammatory diseases that are promoted by emulsifiers and perhaps other modern microbiota stressors.
| S-EPMC10508614 | biostudies-literature