Energy depletion and not ROS formation is a crucial step of glucolipotoxicity (GLTx) in pancreatic beta cells
Author:
Funder
Deutsche Forschungsgemeinschaft
Publisher
Springer Science and Business Media LLC
Subject
Physiology (medical),Clinical Biochemistry,Physiology
Link
http://link.springer.com/article/10.1007/s00424-017-2094-8/fulltext.html
Reference40 articles.
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2. Bindokas VP, Kuznetsov A, Sreenan S, Polonsky KS, Roe MW, Philipson LH (2003) Visualizing superoxide production in normal and diabetic rat islets of Langerhans. J Biol Chem 278(11):9796–9801. https://doi.org/10.1074/jbc.M206913200
3. Brun T, Maechler P (2016) Beta-cell mitochondrial carriers and the diabetogenic stress response. Biochim Biophys Acta 1863(10):2540–2549. https://doi.org/10.1016/j.bbamcr.2016.03.012
4. Cerqueira FM, Chausse B, Baranovski BM, Liesa M, Lewis EC, Shirihai OS, Kowaltowski AJ (2016) Diluted serum from calorie-restricted animals promotes mitochondrial beta-cell adaptations and protect against glucolipotoxicity. FEBS J 283(5):822–833. https://doi.org/10.1111/febs.13632
5. Drews G, Bauer C, Edalat A, Düfer M, Krippeit-Drews P (2015) Evidence against a Ca(2+)-induced potentiation of dehydrogenase activity in pancreatic beta-cells. Pflugers Arch 467(11):2389–2397. https://doi.org/10.1007/s00424-015-1707-3
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1. Nutrient Metabolism, Subcellular Redox State, and Oxidative Stress in Pancreatic Islets and β-Cells;Journal of Molecular Biology;2020-03
2. Nrf2 Activation Protects Mouse Beta Cells from Glucolipotoxicity by Restoring Mitochondrial Function and Physiological Redox Balance;Oxidative Medicine and Cellular Longevity;2019-11-11
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