| Autor: |
Walder, Ken, Kantham, Lakshmi, McMillan, Janine S, Trevaskis, James, Kerr, Lyndal, Silva, Andrea de, Sunderland, Terry, Godde, Nathan, Gao, Yuan, Bishara, Natalie, Windmill, Kelly, Tenne-Brown, Janette, Augert, Guy, Zimmet, Paul Z, Collier, Greg R, De Silva, Andrea |
| Předmět: |
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| Zdroj: |
Diabetes; Jun2002, Vol. 51 Issue 6, p1859-1866, 8p, 2 Diagrams, 1 Chart, 5 Graphs |
| Abstrakt: |
Here we describe a novel protein, which we have named Tanis, that is implicated in type 2 diabetes and inflammation. In Psammomys obesus, a unique polygenic animal model of type 2 diabetes and the metabolic syndrome, Tanis is expressed in the liver in inverse proportion to circulating glucose (P = 0.010) and insulin levels (P = 0.004) and in direct proportion with plasma triglyceride concentrations (P = 0.007). Hepatic Tanis gene expression was markedly increased (3.1-fold) after a 24-h fast in diabetic but not in nondiabetic P. obesus. In addition, glucose inhibited Tanis gene expression in cultured hepatocytes (P = 0.006) as well as in several other cell types (P = 0.001-0.011). Thus, Tanis seems to be regulated by glucose and is dysregulated in the diabetic state. Yeast-2 hybrid screening identified serum amyloid A (SAA), an acute-phase inflammatory response protein, as an interacting protein of Tanis, and this was confirmed by Biacore experiments. SAA and other acute-phase proteins have been the focus of recent attention as risk factors for cardiovascular disease, and we contend that Tanis and its interaction with SAA may provide a mechanistic link among type 2 diabetes, inflammation, and cardiovascular disease. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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