Abstract
Background and aim: The transcription factor FOXO1 has opposing effects in β-cells: On one hand it transmits pro-apoptotic effects under glucolipotoxic conditions, while on the other hand it promotes cell differentiation and insulin secretion under a non-stress environment. It is currently accepted that palmitate mediated lipotoxicity is accompanied with ER stress. However, several observations also indicate that palmitate induces a nuclear accumulation of FOXO1. Additionally, FOXO1 deletion has been shown to reverse β-cell lipotoxicity in mice. This study aims to analyze the role of FOXO1 in palmitate-induced ER stress and beta-cell failure.
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