Role of Oxidative Stress in Pancreatic β-Cell Dysfunction

2004 ◽  
pp. 168-176 ◽  
Author(s):  
Yoshitaka Kajimoto ◽  
Hideaki Kaneto
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction

Role of oxidative stress, endoplasmic reticulum stress, and c-Jun N-terminal kinase in pancreatic β-cell dysfunction and insulin resistance

2006 ◽  
Vol 38 (5-6) ◽  
pp. 782-793 ◽  
Author(s):  
Hideaki Kaneto ◽  
Yoshihisa Nakatani ◽  
Dan Kawamori ◽  
Takeshi Miyatsuka ◽  
Taka-aki Matsuoka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction

Role of oxidative stress, endoplasmic reticulum stress, and c-Jun N-terminal kinase in pancreatic β-cell dysfunction and insulin resistance

2005 ◽  
Vol 37 (8) ◽  
pp. 1595-1608 ◽  
Author(s):  
Hideaki Kaneto ◽  
Yoshihisa Nakatani ◽  
Dan Kawamori ◽  
Takeshi Miyatsuka ◽  
Taka-aki Matsuoka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction

Role of Oxidative Stress in Pancreatic β-Cell Dysfunction

2004 ◽  
Vol 1011 (1) ◽  
pp. 168-176 ◽  
Author(s):  
YOSHITAKA KAJIMOTO ◽  
HIDEAKI KANETO
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction

Molecular aspects of pancreatic β‐cell dysfunction: Oxidative stress, microRNA, and long noncoding RNA

2018 ◽  
Vol 234 (6) ◽  
pp. 8411-8425 ◽  
Author(s):  
Mohammad Javad Saeedi Borujeni ◽  
Ebrahim Esfandiary ◽  
Azar Baradaran ◽  
Ali Valiani ◽  
Mustafa Ghanadian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Molecular Aspects

scholarly journals Cigarette Smoke Exposure Impairs β-Cell Function Through Activation of Oxidative Stress and Ceramide Accumulation

2019 ◽  
Author(s):  
Xin Tong ◽  
Zunaira Chaudry ◽  
Chih-Chun Lee ◽  
Robert N. Bone ◽  
Sukrati Kanojia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smoking Cessation ◽  
Weight Gain ◽  
Cell Function ◽  
Ex Vivo ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Β Cell Function ◽  
Ceramide Accumulation

ABSTRACTObjectivesEpidemiological studies indicate that first- and second-hand cigarette smoke (CS) exposure are important risk factors for the development of type 2 diabetes (T2D). Additionally, elevated diabetes risk has been reported to occur within a short period of time after smoking cessation, and health risks associated with smoking are increased when combined with obesity. At present, the mechanisms underlying these associations remain incompletely understood. The objective of this study was to test the impact of CS exposure on pancreatic β-cell function using rodent and in vitro models.MethodsBeginning at 8 weeks of age, C57BL/6J mice were concurrently fed high fat-diet (HFD) and exposed to CS for 11 weeks, followed by an additional 11 weeks of smoking cessation with continued HFD exposure. Glucose tolerance testing was performed during CS exposure and during the cessation period. Cultured β-cells (INS-1) and primary islets were exposed ex vivo to CS extract (CSE), and β-cell function and viability were tested. Since CS increases ceramide in lungs cells and these bioactive sphingolipids have been implicated in pancreatic β-cell dysfunction in diabetes, islet and β-cell sphingolipid levels were measured in islets from CS-exposed mice and in CSE-treated islets and INS-1 cells using liquid chromatography-tandem mass spectrometry.ResultsCompared to HFD-fed ambient air-exposed mice, HFD-fed and CS- exposed mice had reduced weight gain and better glucose tolerance during the active smoking period. Following smoking cessation, CS-mice exhibited rapid weight gain and a significantly greater increase in glucose intolerance compared to non-smoking control mice. CS-exposed mice had higher serum proinsulin/insulin ratios, indicative of β-cell dysfunction, significantly lower β-cell mass (p=0.02), and reduced β-cell proliferation (p=0.006), and increased islet ceramide accumulation. Ex vivo exposure of isolated islets to CSE was sufficient to increase islet ceramide accumulation, reduce insulin gene expression and glucose-stimulated insulin secretion, and increase β-cell oxidative and ER stress. Treatment with the antioxidant N-acetylcysteine, markedly attenuated the effects of CSE on ceramide levels, restored β-cell function and survival, and increased cyclin D2 expression, while also reducing activation of β-cell ER and oxidative stress.ConclusionsOur results indicate that CS exposure inhibits insulin production, processing, and secretion and reduced β-cell viability and proliferation. These effects were linked to increased β-cell oxidative and ER stress and ceramide accumulation. Mice fed HFD continued to experience detrimental effects of CS exposure even during smoking cessation. Elucidation of mechanisms by which CS exposure impairs β-cell function in synergy with obesity will help design therapeutic and preventive interventions for both active and former smokers.

Role of Hedgehog Interacting Protein in High-Fat Diet-Mediated Pancreatic β-cell Dysfunction

2018 ◽  
Vol 42 (5) ◽  
pp. S54
Author(s):  
Henry Nchienzia ◽  
Min-Chun Liao ◽  
Xin-Ping Zhao ◽  
Shiao-Ying Chang ◽  
Chao-Sheng Lo ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Pancreatic Β Cell ◽  
High Fat ◽  
Β Cell ◽  
Interacting Protein ◽  
Cell Dysfunction

scholarly journals The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes

2021 ◽  
Vol 22 (4) ◽  
pp. 1509
Author(s):  
Natsuki Eguchi ◽  
Nosratola D. Vaziri ◽  
Donald C. Dafoe ◽  
Hirohito Ichii
Keyword(s):  
Oxidative Stress ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Antioxidative Capacity ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Levels ◽  
Cell Dysfunction ◽  
Elevated Glucose ◽  
Β Cell Function

Diabetes is a chronic metabolic disorder characterized by inappropriately elevated glucose levels as a result of impaired pancreatic β cell function and insulin resistance. Extensive studies have been conducted to elucidate the mechanism involved in the development of β cell failure and death under diabetic conditions such as hyperglycemia, hyperlipidemia, and inflammation. Of the plethora of proposed mechanisms, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and oxidative stress have been shown to play a central role in promoting β cell dysfunction. It has become more evident in recent years that these 3 factors are closely interrelated and importantly aggravate each other. Oxidative stress in particular is of great interest to β cell health and survival as it has been shown that β cells exhibit lower antioxidative capacity. Therefore, this review will focus on discussing factors that contribute to the development of oxidative stress in pancreatic β cells and explore the downstream effects of oxidative stress on β cell function and health. Furthermore, antioxidative capacity of β cells to counteract these effects will be discussed along with new approaches focused on preserving β cells under oxidative conditions.

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