ArticleFrontiers in endocrinology2026
Long-chain saturated free fatty acids induce pancreatic β-cell lipotoxic stress via H
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Type 2 diabetes (T2D) is characterized by progressive pancreatic β-cell dysfunction and loss, driven by chronic exposure to elevated circulating free fatty acids (FFAs). Mitochondria-associated endoplasmic reticulum membranes (MAMs), the specialized contact sites between the endoplasmic reticulum (ER) and mitochondria, regulate cellular metabolism and survival, yet their role in β-cell lipotoxicity remains unclear. Methods: We examined the impact of physiologically relevant long-chain saturated (palmitic and stearic acid) and unsaturated (palmitoleic and oleic acid) FFAs, applied alone or in combination, on MAM formation in insulin-secreting INS-1E cells. ER-mitochondria contacts were quantified by proximity-ligand assay (PLA), transmission electron microscopy and genetically encoded MAM sensors. The role of reactive oxygen species was investigated using the H Results: Saturated FFAs significantly increased ER-mitochondria contacts, whereas unsaturated FFAs had no negative effect and counteracted the saturated FFA-induced MAM formation. Expression of GPx8 suppressed palmitate-induced MAM formation, indicating that H Conclusions: Our data demonstrate that dysregulated MAMs constitute a mechanistic link between saturated-FFA-induced lipotoxic stress and β-cell failure in T2D. Targeting MAM remodeling or the upstream H
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