The chemokine macrophage inflammatory protein-1b response to LPA. MIP-1b is a potent chemoattractant for, and activator of, monocytes, lymphocytes and a wide variety of immune cells. We conclude that LPA5 may mediate a pathway for MC activation in circumstances where cancers or cardiovascular inflammation result in the local production of LPA. Type 2 diabetes is undergoing a global epidemic mainly driven by a concomitant epidemic in obesity. The expanded adipose tissue mass in obesity promotes insulin resistance which, in turn, induces Type 2 diabetes in genetically susceptible individuals. It is also well-established that a preponderance of abdominal fat accumulation, estimated by an expanded waist or waist/hip circumference ratio, is a better marker of the obesity-associated complications, including the Metabolic Syndrome and cardiovas- cular disease than obesity per se. Accumulation of excess lipids in the adipose tissue can, in principle, be induced by an expansion of the number of differentiated adipose cells and/or by adipose cell enlargement. As a group, obese individuals have larger fat cells than non-obese and it has long been known that hypertrophic, rather than hyperplastic, obesity is closely associated with insulin resistance and the various aspects of the Metabolic Syndrome Interestingly,Bemegride Spalding et al. recently showed that the number of abdominal subcuta- neous adipose cells becomes established around puberty and that adipose cell expansion becomes the predominant event for subsequent fat accumulation. However, adult women may still recruit new cells in the femoral/gluteal depot which appears to counteract abdominal adipocyte accumulation and this may contribute to the well-established finding that peripheral obesity is less harmful than abdominal obesity. In order to differentiate between hypertrophic and hyperplastic obesity, Arner et al. conceived the delta-factor as a quantitative statistical marker of inappropriate cell enlargement in relation to amount of body fat. In agreement to these findings, no significant correlation was found between changes of CRP levels over time with changes of insulin levels, HOMA-IR as well as LAR in the present study. Several studies have shown increased LDL-cholesterol and triglyceride levels in human subjects when treated with Tocilizumab. This finding was also observed in our cohort, although the changes did not reach statistical significance. In addition, we also measured Lp levels in response to IL-6 inhibition. High Lp levels haven been found to be associated with an increased cardiovascular risk in human subjects in a metaanalysis including several prospective studies with a total number of 5436 human individuals and a mean follow up-period of 10 years. Interestingly, in this meta-analysis the risk ratio did not change following adjustment for other cardiovascular risk factors suggesting that Lp is an independent risk factor.