ChREBP: A Pivotal Player in Glucose Metabolism and Diabetes Therapeutics

Carbohydrate - responsive element binding protein (ChREBP) is a central transcription factor that integrates glucose availability with lipid metabolism, de novo lipogenesis, and hepatokine secretion. Its ability to sense nutrient signals and orchestrate gene expression highlights its importance in maintaining systemic glucose homeostasis and its relevance as a therapeutic target in type 2 diabetes mellitus (T2DM).

At the same time, ChREBP operates within broader transcriptional and signaling networks involving regulators such as FoxO1 and downstream effectors including thioredoxin-interacting protein (TxNIP). Together, these pathways influence insulin sensitivity, β-cell function, inter-organ communication, and the development of diabetic complications. Advances in epigenetics, functional genomics, and multi-omics profiling are now providing unprecedented insights into these mechanisms, opening new opportunities for therapeutic discovery.

This Research Topic invites studies that advance mechanistic and translational understanding of ChREBP and related transcriptional regulators in the context of diabetes.

Submissions may include, but are not limited to:

- ChREBP-mediated regulation of glucose sensing, de novo lipogenesis, and hepatokine secretion

- Interactions between ChREBP and other transcriptional regulators (e.g., FoxO1) and their effects on systemic metabolism

- Downstream targets of ChREBP such as TxNIP and their role in β-cell dysfunction and insulin resistance

- Crosstalk between nutrient-responsive transcription factors and metabolic signaling pathways (e.g., AMPK, mTOR)

- Epigenetic and genomic regulation of ChREBP and related transcriptional networks

- Insights from transcriptomics, proteomics, and metabolomics into ChREBP-mediated metabolic control

- Applications of emerging technologies (e.g., CRISPR/Cas9, high-throughput screening, multi-omics integration) to dissect transcriptional mechanisms in diabetes

- Contributions of ChREBP and transcriptional dysregulation to diabetic complications, including nephropathy, neuropathy, and retinopathy

- Exploration of transcription factors as therapeutic targets for restoring metabolic balance in T2DM