Chronic exposure to elevated glucose levels and free fatty acids impairs beta-cell function, leading to insulin secretion defects and beta-cell death, potentially prompting diabetes. These effects, referred to as glucolipotoxicity, and mechanisms induced by saturated versus unsaturated fatty acids remain unclear. Here, I investigated the role of the free fatty acid receptor, FFAR1, in INS-1E β-cells chronically exposed to glucose and free fatty acids. Glucose was the main driver for β-cell dysfunction. Free fatty acids exacerbated only some of the glucotoxic effects while partially restoring glucose-stimulated insulin secretion in cells exposed to glucotoxicity. The contribution of intracellular lipids in this process was highlighted. Chronic elevated glucose strongly down-regulated Ffar1 expression in INS-1E β-cells, likely minimizing its role under glucolipotoxic condition. However, in this context, the remaining fraction of FFAR1 may contribute to the partial restoration of β-cell function, notably through the binding of secreted fatty acids from intracellular lipids turnover.