In particular, the mediation of this sub-clinical inflammation in the pathogenesis of Type 2 Diabetes Mellitus (T2DM) is proposed to arise through increasing adiposity [3,4]; with adipose tissue representing a site of an acute phase response [5,6] through the production of known pro-inflammatory adipocytokines such as leptin, tumor necrosis factor (TNF-α) and interleukin (IL-6), amongst others [7-9]. This evidence concerns the gene IL6 and type 2 diabetes mellitus.