Tanis: a link between type 2 diabetes and inflammation?

Walder, Ken, Kantham, Lakshmi, McMillan, Janine, Trevaskis, James, Kerr, Lyndal, de Silva, Andrea, Sunderland, Terry, Godde, Nathan, Gao, Yuan, Bishara, Natalie, Windmill, Kelly, Tenne-Brown, Janette, Augert, Guy, Zimmet, Paul and Collier, Greg 2002, Tanis: a link between type 2 diabetes and inflammation?, Diabetes, vol. 51, no. 6, pp. 1859-1866.

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Title Tanis: a link between type 2 diabetes and inflammation?
Author(s) Walder, Ken
Kantham, Lakshmi
McMillan, Janine
Trevaskis, James
Kerr, Lyndal
de Silva, Andrea
Sunderland, Terry
Godde, Nathan
Gao, Yuan
Bishara, Natalie
Windmill, Kelly
Tenne-Brown, Janette
Augert, Guy
Zimmet, Paul
Collier, Greg
Journal name Diabetes
Volume number 51
Issue number 6
Start page 1859
End page 1866
Publisher American Diabetes Association
Place of publication New York, N.Y.
Publication date 2002-06
ISSN 0012-1797
1939-327X
Summary 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.
Notes RSD author affiliation updated GH 29 April 2011
Language eng
Field of Research 060199 Biochemistry and Cell Biology not elsewhere classified
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2002, American Diabetes Association
Persistent URL http://hdl.handle.net/10536/DRO/DU:30001597

Document type: Journal Article
Collections: School of Exercise and Nutrition Sciences
School of Health Sciences
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