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Role Of FFAR1 in the response of INS-1E β-cells to glucolipotoxicity

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Defense Thèse de doctorat : Univ. Genève, 2019 - Sc. Vie - Pharma 12 - 2019/03/26
Abstract 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.
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URN: urn:nbn:ch:unige-1172968
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OBERHAUSER, Lucie. Role Of FFAR1 in the response of INS-1E β-cells to glucolipotoxicity. Université de Genève. Thèse, 2019. https://archive-ouverte.unige.ch/unige:117296

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Deposited on : 2019-05-13

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