News Release

Improved insulin signaling reduces atherosclerosis in mouse models

Peer-Reviewed Publication

JCI Journals

Patients with diabetes and metabolic syndrome are at increased risk of atherosclerosis and subsequent heart disease. It is not fully understood why atherosclerosis is increased with diabetes, but it has been proposed that insulin resistance in endothelial cells, which line blood vessels, promotes inflammation. In this issue of JCI Insight, a team led by George King of Harvard Medical School shows that increased insulin signaling in the endothelium of atherosclerosis-prone mice reduces development of disease and improves aorta function. The anti-atherogenic effects of insulin were linked to induction of nitric oxide and activation of downstream pathways, including endothelin receptor B (EDNRB). EDNRB was decreased in arteries from patients with diabetes. In a murine model, loss of EDNRB accelerated atherosclerosis, even in animals with enhanced insulin signaling. Together, the results of this study suggest that strategies to improve insulin signaling in endothelial cells have the potential to reduce diabetes-associated atherosclerosis.

###

TITLE:

Insulin decreases atherosclerosis by inducing endothelin receptor B expression

AUTHOR CONTACT:

George King
Joslin Diabetes Center
Email: george.king@joslin.harvard.edu

View this article at: http://insight.jci.org/articles/view/86574?key=5315956643073be267d8

JCI Insight is the newest publication from the American Society of Clinical Investigation, a nonprofit honor organization of physician-scientists. JCI Insight is dedicated to publishing a range of translational biomedical research with an emphasis on rigorous experimental methods and data reporting. All articles published in JCI Insight are freely available at the time of publication. For more information about JCI Insight and all of the latest articles go to http://www.insight.jci.org.


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.