Journal
MOLECULAR ENDOCRINOLOGY
Volume 25, Issue 3, Pages 492-502Publisher
OXFORD UNIV PRESS INC
DOI: 10.1210/me.2010-0224
Keywords
-
Categories
Funding
- National Institutes of Health [DK 62071]
- Department of Defense [W81XWH-0510387]
- Veterans Administration Merit Review
- [HL 77419]
Ask authors/readers for more resources
Acute insulin resistance is common after injury, infection, and critical illness. To investigate the role of reactive oxygen species (ROS) in critical illness diabetes, we measured hepatic ROS, which rapidly increased in mouse liver. Overexpression of superoxide dismutase 2, which decreased mitochondrial ROS levels, protected mice from the development of acute hepatic insulin resistance. Insulin-induced intracellular signaling was dramatically decreased, and cellular stress signaling was rapidly increased after injury, resulting in the hyperglycemia of critical illness diabetes. Insulin-induced intracellular signaling, activation of stress (c-Jun N-terminal kinase) signaling, and glucose metabolism were all normalized by superoxide dismutase 2 overexpression or by pretreatment with antioxidants. Thus, ROS play an important role in the development of acute hepatic insulin resistance and activation of stress signaling after injury. (Molecular Endocrinology 25: 492-502, 2011)
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available