Tanis: A link between type 2 diabetes and inflammation?

Ken Walder, Lakshmi Kantham, Janine S. McMillan, James Trevaskis, Lyndal Kerr, Andrea De Silva, Terry Sunderland, Nathan Godde, Yuan Gao, Natalie Bishara, Kelly Windmill, Janette Tenne-Brown, Guy Augert, Paul Z. Zimmet, Greg R. Collier

Research output: Contribution to journalArticleResearchpeer-review

133 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1859-1866
Number of pages8
JournalDiabetes
Volume51
Issue number6
DOIs
Publication statusPublished - 2002
Externally publishedYes

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