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Protein Kinase C-β Contributes to Impaired Endothelial Insulin Signaling in Humans With Diabetes Mellitus
Author(s) -
Corey E. Tabit,
Sherene M. Shenouda,
Monica Holbrook,
Jessica L. Fetterman,
Soroosh Kiani,
Alissa A. Frame,
Matthew A. Kluge,
Aaron Held,
Mustali M. Dohadwala,
Noyan Gokce,
Melissa G. Farb,
James L. Rosenzweig,
Neil B. Ruderman,
Joseph A. Vita,
Naomi M. Hamburg
Publication year - 2012
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.112.127514
Subject(s) - medicine , endocrinology , enos , diabetes mellitus , insulin resistance , endothelial dysfunction , insulin , protein kinase c , endothelium , type 2 diabetes mellitus , nitric oxide , phosphorylation , nitric oxide synthase , biology , microbiology and biotechnology
Abnormal endothelial function promotes atherosclerotic vascular disease in diabetes. Experimental studies indicate that disruption of endothelial insulin signaling, through the activity of protein kinase C-β (PKCβ) and nuclear factor κB, reduces nitric oxide availability. We sought to establish whether similar mechanisms operate in the endothelium in human diabetes mellitus.

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