Long term liver specific glucokinase gene defect induced diabetic cardiomyopathy by up regulating NADPH oxidase and down regulating insulin receptor and p-AMPK
Conclusions:
Our results indicate that changes in the myocardium occur in the liver-specific glucokinase knockout mouse and suggest that reduced glucokinase expression in the liver may induce diabetic cardiomyopathy by up regulating NADPH oxidase and down regulating insulin receptor and p-AMPK protein levels. Rosiglitazone treatment may protect against diabetic cardiomyopathy by altering the levels of a set of proteins involved in cardiac damage.
Source: Cardiovascular Diabetology - Category: Cardiology Authors: Hui LiXi WangYiqing MaoRuobi HuWei XuZhen LeiNa ZhouLing JinTingting GuoZhixin LiDavid IrwinGang NiuHuanran Tan Source Type: research
More News: Avandia | Cardiology | Cardiomyopathy | Cardiovascular | Diabetes | Electrocardiogram | Endocrinology | Genetics | Heart | Insulin | Liver | Mitochondria | Study | Urology & Nephrology