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Cited by 1,435

The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.

Oxidative stress, insulin signaling, and diabetes

Open access
Rains, Justin L., Jain, Sushil K.·2011·Free Radical Biology and Medicine
DOI 10.1016/j.freeradbiomed.2010.12.006
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Abstract

Oxidative stress has been implicated as a contributor to both the onset and the progression of diabetes and its associated complications. Some of the consequences of an oxidative environment are the development of insulin resistance, β-cell dysfunction, impaired glucose tolerance, and mitochondrial dysfunction, which can lead ultimately to the diabetic disease state. Experimental and clinical data suggest an inverse association between insulin sensitivity and ROS levels. Oxidative stress can arise from a number of different sources, whether disease state or lifestyle change, including episodes of ketosis, sleep restriction, and excessive nutrient intake. Oxidative stress activates a series of stress pathways involving a family of serine/threonine kinases which in turn have a negative effect on insulin signaling. More experimental evidence is needed to pinpoint the mechanisms contributing to insulin resistance in both type 1 diabetics and non-diabetic individuals. Oxidative stress can be reduced by controlling hyperglycemia and calorie intake. Overall, this review outlines various mechanisms that lead to the development of oxidative stress. Intervention and therapy that alters or disrupts these mechanisms may serve to reduce the risk of insulin resistance and the development of diabetes.

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Metadata

Authors
Rains, J. L., & Jain, S. K.
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
2011-03
Volume
50
Issue
5
Pages
567-575
ISSN
0891-5849 (ISSN-L)
DOI
10.1016/j.freeradbiomed.2010.12.006
OpenAlex
W2064483915
Cited by
1,435
References
27
FWCI
21.15
Type
journal article
Language
en
Open access
green

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