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The Sulfur-Insulin Deformation Hypothesis redefines T2DM by asserting that sulfur deficiency, stemming from mitochondrial dysfunction in intestinal epithelial cells, drives insulin misfolding, a primary trigger of insulin resistance

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In mice and rats, three distinct GPx4 isoforms, cytosolic GPx4, mitochondrial GPx4 (mGPx4), and nuclear GPx4 (nGPx4), were identified with different functions