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REDD2 Activation Exacerbates Pancreatic β-Cell Dysfunction and Holds Biomarker Potential

Metabolic stress triggers REDD2 to block mTORC1 signaling, undermining β-cell survival

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Overview

  • Exposure to high glucose, fatty acids and diabetogenic agents markedly upregulates REDD2 transcription in pancreatic β-cells
  • Experimental knockdown of REDD2 preserves insulin secretion and enhances β-cell survival under metabolic strain
  • REDD2-deficient mice fed a high-fat diet or treated with diabetes-inducing chemicals maintain better blood sugar control and β-cell mass
  • Analysis of human islet cells reveals higher REDD2 levels correlate with reduced β-cell functional capacity
  • Targeting REDD2 with small molecule inhibitors, genetic methods or functional dietary components offers a novel strategy to prevent or delay type 2 diabetes