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Our model predicts outcomes very well

Egr-1 has been implicated in the onset of insulin-resistance, as previous studies in insulin-resistant T2DM mice identified that loss of function in Egr-1 restores insulin sensitivity via increased phosphorylation of the insulin receptor substrate-1 tyrosine kinase [32]

In research models, this creates a broader regenerative response profile

Its imbalanced receptor affinity and biased signaling provide enhanced insulin secretion and improved metabolic outcomes beyond selective GLP-1 agonism

Nucleic Acids Res 46 , W296w303 (2018)

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