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Glucolipotoxicity promotes the capacity of the glycerolipid/NEFA cycle supporting the secretory response of pancreatic beta cells – published online 12/01/2022

Oberhauser graphical abstract

Lucie Oberhauser, Cecilia Jiménez-Sánchez, Jesper Grud Skat Madsen, Dominique Duhamel, Susanne Mandrup, Thierry Brun, Pierre Maechler

About three decades ago, in the context of type 2 diabetes, the concept of lipotoxicity, and later of glucolipotoxicity, was applied to pancreatic beta cells. However, after all these years it remains debated whether essential components of the organ’s chemistry, namely fat and sugar, could be qualified as genuine toxic molecules. In this issue, Oberhauser et al ( report results from a study in which they exposed pancreatic islets to various so-called glucolipotoxic culture conditions before analysing their response to standard conditions of glucose-stimulated insulin secretion. The authors report that high glucose, rather than glucose per se, is detrimental for beta cell function. Cells exposed to fatty acids and high glucose exhibited massive fat storage, which was rapidly mobilised upon return to normal conditions. Such fat turnover was instrumental for the preservation of the secretory response in cells experiencing glucotoxicity. The authors conclude that these findings advocate against continuous energy-rich snacking without fasting periods for the preservation of beta cell function.

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