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The constant levels of marker proteins such as GAPDH, combined with observations indicating that knockdown of the UPR element, BiP/Grp78 , revealed no detectable effects on Nrf2, GCLC, or glutathione, further support the conclusion that NFT-mediated stabilization of Nrf2 is a major contributor to its accumulation and the subsequent stimulation of GCL and glutathione synthesis

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Furthermore, it is possible that somatostatin directly inhibits glucagon secretion by binding to its receptor in the alpha cell, since GLP- 1 stimulates islet somatostatin secretion directly through the canonical GLP- 1 receptor, expressed on delta cells [71]