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Dietary intervention preserves β cell function in mice through CTCF-mediated transcriptional reprogramming
Ruo-Ran Wang1,2,3, Xinyuan Qiu1,4, Ran Pan1,2,3
1Department of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
The Journal of Experimental Medicine
|June 2, 2022
Summary
Dietary intervention reverses type 2 diabetes (T2D) progression by restoring pancreatic beta cell function. This involves reversing changes in gene expression and chromatin accessibility, with CTCF playing a key role.
Area of Science:
- Endocrinology
- Metabolic Diseases
- Molecular Biology
Background:
- Pancreatic beta cell plasticity is crucial for type 2 diabetes (T2D) progression and remission.
- The adaptive mechanisms of beta cells during T2D remain incompletely understood.
Purpose of the Study:
- To investigate beta cell adaptation to high-fat diet (HFD) feeding, from compensation to decompensation.
- To identify molecular mechanisms underlying beta cell dysfunction and potential therapeutic targets.
Main Methods:
- Establishment of a mouse model mimicking HFD-induced beta cell adaptation.
- Comprehensive islet functional assays and transcriptome analysis.
- ATAC-seq for chromatin accessibility profiling and motif analysis.
Main Results:
- HFD feeding induced dynamic changes in beta cell transcriptome and chromatin remodeling.
- Prediabetic dietary intervention fully rescued beta cell dysfunction and reversed HFD-induced molecular changes.
- CTCF was identified as a key regulator, with its restoration ameliorating beta cell dysfunction.
Conclusions:
- Beta cell plasticity is dynamically regulated by transcriptional networks and chromatin remodeling.
- Dietary interventions can reverse T2D-associated beta cell dysfunction.
- CTCF is a critical mediator of beta cell adaptation and a potential therapeutic target for T2D.
