Journal ArticleDOI
Dietary Zinc Supplementation Inhibits NFκB Activation and Protects Against Chemically Induced Diabetes in CD1 Mice
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TLDR
High zinc intake significantly reduced the severity of Type I diabetes in alloxan and streptozotocin-induced diabetic models and inhibited NFκB activation and decreased the expression of inducible NO synthase, a downstream target gene ofNFκB.Abstract:
Zinc status in patients with Type I diabetes is significantly lower than healthy controls. Whether zinc supplementation can prevent the onset of Type I diabetes is unknown. Recent studies have suggested that the generation of reactive oxygen species (ROS) is a cause of β cell death leading to Type I diabetes. In addition, we found that activation of NFκB (a ROS-sensitive transcription factor that regulates immune responses) may be the key cellular process that bridges oxidative stress and the death of β cells. Zinc is a known antioxidant in the immune system. Therefore, this study is designed to test whether an increase in dietary zinc can prevent the onset of Type I diabetes by blocking NFκB activation in the pancreas. The results show that high zinc intake significantly reduced the severity of Type I diabetes (based on hyperglycemia, insulin level, and Islet morphology) in alloxan and streptozotocin-induced diabetic models. Zinc supplementation also inhibited NFκB activation and decreased the expression...read more
Citations
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Journal ArticleDOI
Oxidative Stress and Stress-Activated Signaling Pathways: A Unifying Hypothesis of Type 2 Diabetes
TL;DR: A unifying hypothesis is proposed whereby hyperglycemia and FFA-induced activation of the nuclear factor-kappaB, p38 MAPK, and NH2-terminal Jun kinases/stress-activated protein kinases stress pathways plays a key role in causing late complications in type 1 and type 1 diabetes, along with insulin resistance and impaired insulin secretion in type 2 diabetes.
Journal ArticleDOI
Zinc in human health: effect of zinc on immune cells.
TL;DR: The studies in the cell culture models showed that the activation of many zinc-dependent enzymes and transcription factors were adversely affected due to zinc deficiency, and zinc supplementation decreased oxidative stress markers and generation of inflammatory cytokines.
Journal ArticleDOI
Timing of Initial Cereal Exposure in Infancy and Risk of Islet Autoimmunity
Jill M. Norris,Katherine J. Barriga,Georgeanna J. Klingensmith,Michelle Hoffman,George S. Eisenbarth,Henry A. Erlich,Marian Rewers +6 more
TL;DR: There may be a window of exposure to cereals in infancy outside which initial exposure increases IA risk in susceptible children, and this study is the first to examine this window.
Journal ArticleDOI
Antioxidant effect of zinc in humans.
TL;DR: The results suggest that zinc supplementation may lead to down regulation of the inflammatory cytokines through upregulation of the negative feedback loop A20 to inhibit induced NF-kappaB activation.
Journal ArticleDOI
Zinc deficiency, DNA damage and cancer risk.
TL;DR: This review will focus on potential mechanisms by which zinc deficiency impairs host protective mechanisms designed to protect against DNA damage, enhances susceptibility to DNA-damaging agents and ultimately increases risk for cancer.
References
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Journal ArticleDOI
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TL;DR: Not only are oxygen radicals involved in the cause of diabetes, they also appear to play a role in some of the complications seen in long-term treatment of diabetes.
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