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However, under stress conditions, modifications of KEAP1 disrupt this interaction, allowing NRF2 to accumulate and translocate into the nucleus

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While most of the actions of metformin appear to be mediated by cellular activation of AMP-activated protein kinase (AMPK), their findings indicate that the effects on incretin receptor expression in beta cells appear to be independent of AMPK, but, rather, are mediated by peroxisome proliferator-activated receptor (PPAR), as metformin failed to induce expression of the gene encoding the incretin receptor in islets from Ppar knockout mice [10]