Tanis: a link between type 2 diabetes and inflammation?
Version 2 2024-06-17, 03:50Version 2 2024-06-17, 03:50
Version 1 2014-10-27, 16:26Version 1 2014-10-27, 16:26
journal contribution
posted on 2024-06-17, 03:50authored byKen WalderKen Walder, L Kantham, J McMillan, J Trevaskis, L Kerr, A de Silva, T Sunderland, N Godde, Y Gao, N Bishara, Kelly WindmillKelly Windmill, J Tenne-Brown, G Augert, P Zimmet, G Collier
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.