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RNA-seq of primary islets in HFD_DMSO，HFD_CGP and ND mice

ABSTRACT: RNA-seq of primary islets in HFD_DMSO，HFD_CGP and ND mice

PROVIDER: PRJNA745471 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15097841_1.fastq.gz	Fastqsanger.gz
	SRR15097841_2.fastq.gz	Fastqsanger.gz
	SRR15097842_1.fastq.gz	Fastqsanger.gz
	SRR15097842_2.fastq.gz	Fastqsanger.gz
	SRR15097843_1.fastq.gz	Fastqsanger.gz

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RNA-seq of primary islets in HFD_DMSO，HFD_CGP and ND mice

Project description:We investigated the underlying molecular mechanism of CGP 57380's effects in type 2 diabetes by comparing gene expression of whole primary islets isolated from HFD_DMSO,HFD_CGP and ND mice by RNA sequencing.C57BL/6 mice were fed an HFD for 4 months and then oral gavage DMSO and CGP 57380 for about 1 month separately to studied gene-expression differences resulting in HFD-induced hyperinsulinemia and metabolic abnormities.At the same time ,explore the therapeutic effect of CGP 57380 on type 2 diabetes,and the changes in the signal pathways in it.Gene set-enrichment ananlysis was performed using Kyoto Encyclopedia of Genomes algorithms and MSigDB software.The most enriched pathways were linked to pathyways associated with PI3K-Akt signaling pathway, pancreatic secretion and NF-kappa B signaling pathway.

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Project description:Type 2 diabetes is associated with defective insulin secretion and reduced β-cell mass. Available treatments provide a temporary reprieve, but secondary failure rates are high, making insulin supplementation necessary. Reversibility of b-cell failure is a key translational question. Here, we reverse-engineered and interrogated pancreatic islet-specific regulatory networks to discover T2D-specific subpopulations characterized by metabolic-inflexibility and endocrine-progenitor/stem cell features. Single-cell gain- and loss-of-function and glucose-induced Ca++ flux analyses of top candidate MR in islet cells validated transcription factor BACH2 and associated epigenetic effectors as a key driver of T2D cell states. BACH2 knockout in T2D islets reversed cellular features of the disease, restoring a non-diabetic phenotype. BACH2-immunoreactive islet cells increased ~4-fold in diabetic patients, confirming the algorithmic prediction of clinically relevant subpopulations. Treatment with a BACH inhibitor lowered glycemia and increased plasma insulin levels in diabetic mice, and restored insulin secretion in diabetic mice and human islets. The findings suggest that T2D-specific populations of failing b-cells can be reversed and indicate pathways for pharmacological intervention, including via BACH2 inhibition.

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