scholarly journals Antioxidation of Cerium Oxide Nanoparticles to Several Series of Oxidative Damage Related to Type II Diabetes Mellitus In Vitro

2016 ◽  
Vol 22 ◽  
pp. 3792-3797 ◽  
Author(s):  
Jing-hui Zhai ◽  
Yi Wu ◽  
Xiao-ying Wang ◽  
Yue Cao ◽  
Kan Xu ◽  
...  
2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Joshua A. David ◽  
William J. Rifkin ◽  
Piul S. Rabbani ◽  
Daniel J. Ceradini

Despite improvements in awareness and treatment of type II diabetes mellitus (TIIDM), this disease remains a major source of morbidity and mortality worldwide, and prevalence continues to rise. Oxidative damage caused by free radicals has long been known to contribute to the pathogenesis and progression of TIIDM and its complications. Only recently, however, has the role of the Nrf2/Keap1/ARE master antioxidant pathway in diabetic dysfunction begun to be elucidated. There is accumulating evidence that this pathway is implicated in diabetic damage to the pancreas, heart, and skin, among other cell types and tissues. Animal studies and clinical trials have shown promising results suggesting that activation of this pathway can delay or reverse some of these impairments in TIIDM. In this review, we outline the role of oxidative damage and the Nrf2/Keap1/ARE pathway in TIIDM, focusing on current and future efforts to utilize this relationship as a therapeutic target for prevention, prognosis, and treatment of TIID.


FEBS Letters ◽  
1999 ◽  
Vol 448 (1) ◽  
pp. 120-122 ◽  
Author(s):  
Almas Rehman ◽  
Jaffar Nourooz-Zadeh ◽  
Wenke Möller ◽  
Hans Tritschler ◽  
Paulo Pereira ◽  
...  

2000 ◽  
Vol 18 ◽  
pp. S144
Author(s):  
R. García-Robles ◽  
F. Villalba-Díaz ◽  
O. González-Albarrán ◽  
S. Calvo ◽  
O. Gómez ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Fauze Camargo Maluf ◽  
David Feder ◽  
Alzira Alves de Siqueira Carvalho

In the early sixties, a discussion started regarding the association between Parkinson’s disease (PD) and type II diabetes mellitus (T2DM). Today, this potential relationship is still a matter of debate. This review aims to analyze both diseases concerning causal relationships and treatments. A total of 104 articles were found, and studies on animal and “in vitro” models showed that T2DM causes neurological alterations that may be associated with PD, such as deregulation of the dopaminergic system, a decrease in the expression of peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α), an increase in the expression of phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes 15 (PED/PEA-15), and neuroinflammation, as well as acceleration of the formation of alpha-synuclein amyloid fibrils. In addition, clinical studies described that Parkinson’s symptoms were notably worse after the onset of T2DM, and seven deregulated genes were identified in the DNA of T2DM and PD patients. Regarding treatment, the action of antidiabetic drugs, especially incretin mimetic agents, seems to confer certain degree of neuroprotection to PD patients. In conclusion, the available evidence on the interaction between T2DM and PD justifies more robust clinical trials exploring this interaction especially the clinical management of patients with both conditions.


1997 ◽  
Vol 56 ◽  
pp. 482
Author(s):  
M. Horváth ◽  
Cs. Keszthelyi ◽  
M.N. Vers ◽  
P. Kempler ◽  
A. Marton ◽  
...  

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