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Nutrient Metabolism, Subcellular Redox State, and Oxidative Stress in Pancreatic Islets and β-Cells. | LitMetric

Nutrient Metabolism, Subcellular Redox State, and Oxidative Stress in Pancreatic Islets and β-Cells.

J Mol Biol

Université Catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Avenue Hippocrate 55 (B1.55.06), B-1200 Brussels, Belgium. Electronic address:

Published: March 2020

AI Article Synopsis

  • Insulin-secreting β-cells in the pancreas are crucial for regulating blood sugar levels and are impacted by insulin resistance, leading to type 2 diabetes (T2D).
  • Reactive oxygen species (ROS) can both aid insulin secretion and negatively affect cell survival in T2D, raising debate on whether reducing oxidative stress might hinder insulin release.
  • Recent advancements in genetically-encoded redox probes have revealed that the relationship between nutrients, β-cell redox changes, and ROS toxicity is more intricate than previously recognized, highlighting the importance of subcellular processes in understanding these mechanisms.

Article Abstract

Insulin-secreting pancreatic β-cells play a critical role in blood glucose homeostasis and the development of type 2 diabetes (T2D) in the context of insulin resistance. Based on data obtained at the whole cell level using poorly specific chemical probes, reactive oxygen species (ROS) such as superoxide and hydrogen peroxide have been proposed to contribute to the stimulation of insulin secretion by nutrients (positive role) and to the alterations of cell survival and secretory function in T2D (negative role). This raised the controversial hypothesis that any attempt to decrease β-cell oxidative stress and apoptosis in T2D would further impair insulin secretion. Over the last decade, the development of genetically-encoded redox probes that can be targeted to cellular compartments of interest and are specific of redox couples allowed the evaluation of short- and long-term effects of nutrients on β-cell redox changes at the subcellular level. The data indicated that the nutrient regulation of β-cell redox signaling and ROS toxicity is far more complex than previously thought and that the subcellular compartmentation of these processes cannot be neglected when evaluating the mechanisms of ROS production or the efficacy of antioxidant enzymes and antioxidant drugs under glucolipotoxic conditions and in T2D. In this review, we present what is currently known about the compartmentation of redox homeostatic systems and tools to investigate it. We then review data about the effects of nutrients on β-cell subcellular redox state under normal conditions and in the context of T2D and discuss challenges and opportunities in the field.

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Source
http://dx.doi.org/10.1016/j.jmb.2019.10.012DOI Listing

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