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The effects of antioxidants on insulin signaling in spontaneously hypertensive rat vascular smooth muscle cells
Author(s) -
Gardner Carla,
Motley Evangeline,
Washington Benny
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1226.37
Subject(s) - protein kinase b , insulin receptor , insulin , reactive oxygen species , insulin receptor substrate , pyrrolidine dithiocarbamate , phosphorylation , irs1 , insulin resistance , medicine , endocrinology , signal transduction , proto oncogene proteins c akt , pi3k/akt/mtor pathway , chemistry , biochemistry , nf κb
The objective of this study was to investigate the possible role of reactive oxygen species on insulin signaling in a hypertensive rat model. Because Protein kinase B/Akt serves as a link between upstream insulin signals, such as insulin receptor substrate‐1 and their cellular consequences, we sought to determine the phosphorylative characteristics of Akt in the insulin signaling pathway. To elucidate the effects of reactive oxygen species, spontaneously hypertensive vascular smooth muscle cells were treated with 6.25–50 μM hydrogen peroxide (H 2 O 2 ). Our results indicated that 6.25 μM H 2 O 2 enhanced Akt phosphorylation, while 25 μM decreased insulin‐induced Akt phosphorylation. We also demonstrated that H 2 O 2 decreased insulin receptor substrate‐1 phosphorylation. Further, H 2 O 2 ‐induced inhibition of insulin signaling was inhibited by the antioxidant, pyrrolidine dithiocarbamate. These studies provide more evidence that reactive oxygen species inhibit insulin signal transduction thereby causing insulin resistance leading to cardiovascular disease. This work was supported by a grant from the Faculty Research Award program of the Division of Research and Sponsored Programs, Tennessee State University.