Fig. 9: ChREBPβ is required for adaptive β-cell expansion but contributes to glucose toxicity with prolonged hyperglycemia and effects of its overexpression can be rescued by activation of the Nrf2 antioxidant pathway.
From: Maladaptive positive feedback production of ChREBPβ underlies glucotoxic β-cell failure
Nuclear expression of ChREBPβ increases in β-cells with increased glucose concentrations. Loss of function experiments demonstrate that ChREBPβ is necessary for adaptive expansion of β-cells after a high fat diet. Gain of function experiments demonstrate that ChREBPβ overexpression mimics glucose toxicity. Deletion of ChREBPβ protects β-cells from glucolipotoxicity and ChREBPβ-mediated β-cell death can be mitigated by overexpression of ChREBPα or by activation of the Nrf2 antioxidant pathway. Created with BioRender.com.
