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Low-Level Arsenic Impairs Glucose-Stimulated Insulin Secretion in Pancreatic Beta Cells: Involvement of Cellular Adaptive Response to Oxidative Stress
Author(s) -
Jingqi Fu,
Courtney G. Woods,
Einav YehudaShnaidman,
Qiang Zhang,
Victoria Wong,
Sheila Collins,
Guifan Sun,
Melvin E. Andersen,
Jingbo Pi
Publication year - 2010
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.0901608
Subject(s) - oxidative stress , arsenite , sodium arsenite , endocrinology , reactive oxygen species , medicine , intracellular , glutathione , carbohydrate metabolism , arsenic toxicity , biology , antioxidant , insulin , chemistry , biochemistry , arsenic , toxicity , enzyme , organic chemistry
Chronic exposure of humans to inorganic arsenic, a potent environmental oxidative stressor, is associated with incidence of type 2 diabetes (T2D). A key driver in the pathogenesis of T2D is impairment of pancreatic beta-cell function, with the hallmark of beta-cell function being glucose-stimulated insulin secretion (GSIS). Reactive oxygen species (ROS) derived from glucose metabolism serve as one of the metabolic signals for GSIS. Nuclear factor-erythroid 2-related factor 2 (Nrf2) is a central transcription factor regulating cellular adaptive response to oxidative stress.

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