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:Type 1 diabetes mellitus (T1D) is caused by killing of insulin producing β cells by CD8+T cells. The disease progression accelerates as glucose tolerance deteriorates suggesting that acquired factors contribute. To identify how environmental factors may lead to the expansion and pathogenicity of the diabetogenic T cells, we analyzed diabetogenic NRP-V7-reactive CD8+ T cells that recognize a peptide from the diabetes antigen IGRP in prediabetic NOD mice. There was an increase in the frequency of the NRP-V7-reactive cells coinciding with the time of glucose intolerance. The T cells persisted in hyperglycemic NOD mice maintained with an insulin pellet despite destruction of beta cells. We compared gene expression in the NRP-V7-reactive T cells to others that shared their phenotype but not selected for reactivity to diabetes antigens viral antigen reactive cells. Compared to these other cells, the NRP-V7-reactive cells exhibited gene expression of memory precursor effector cells. They had reduced cellular proliferation and were less dependent on oxidative phosphorylation. When prediabetic NOD mice were treated with 2DG to block aerobic glycolysis, there was a reduction in the diabetes antigen vs other cells of similar phenotype and loss of lymphoid cells infiltrating the islets. In addition, treatment of NOD mice with 2DG resulted in improved cell granularity. These findings identify a link between metabolic disturbances and autoreactive T cells that promotes development of autoimmune diabetes.
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