Since the cytokines causing classical autoimmune diseases like rheumatoid arthritis are also thought to promote low-grade inflammation in the pathogenesis of insulin resistance and type 2 diabetes, clinical investigation of the effects of TNF-a and interleukin-1 inhibitors in human subjects on metabolic parameters has previously been undertaken. For example, Rosenvinge A. et al. examined insulin sensitivity by hyperinsulinaemic euglycaemic clamp studies in patients with rheumatoid arthritis before and 8 weeks after adalimumab treatment. Interestingly, they did not observe a significant effect of anti-TNF-a treatment on insulin sensitivity. This finding has been confirmed by Dominguez et al. in a cohort of 20 obese patients with type 2 diabetes where etanercept treatment did not affect insulin sensitivity. These observations raise the question, whether low-grade inflammation is important at all in the development of type 2 diabetes in the human organism or if elevated inflammatory markers are only epiphenom- ena. However, in a double-blinded, parallel-group trial involving 70 patients with type 2 diabetes anakinra treatment for 13 weeks lowered glycosylated haemoglobin-A1c levels by 0.46% compared to placebo. Interestingly, Pyriproxyfen this improvement of glycemic control was not due to enhanced insulin sensitivity but rather due to improved b-cell secretory function suggesting that IL-1 is more involved in maintaining b-cell homeostasis than in adipose tissue biology in human subjects with type 2 diabetes. Of the many interleukins identified, IL-6 exhibits a strong association with insulin resistance in human subjects. In 2009 a monoclonal antibody against the IL-6 receptor, called Tocilizumab, was approved for treatment of rheumatoid arthritis in Europe. Since Povidone iodine translational research within the last few years failed to demonstrate an important role for TNF-a in inducing insulin resistance in humans, in the present study we aimed to examine if IL-6 might be of clinical relevance in this context by measuring insulin sensitivity, adipokine serum levels and lipid parameters in patients with immunological disease before and at 1 and 3 months of Tocilizumab therapy. Of importance, the patients were advised not to change the steroid dosage throughout the study period to ensure the metabolic effects observed are solely due to Tocilizumab. After the first month of treatment the HOMA-IR did not significantly change compared to baseline. However, at the end of the study period the HOMA-IR significantly decreased, indicating enhanced insulin sensitivity due to inhibition of IL-6 signalling. To substantiate this finding we also calculated the LAR, a novel marker for insulin resistance. In complete agreement with the HOMA-IR, the LAR was unaltered within the first month of the study period but was significantly reduced after 3 months of Tocilizumab therapy. Mean glycosylated HbA1c levels of these non-diabetic patients were within the normal range at baseline and did not change significantly throughout the study period. Taken together, the two independent parameters, HOMA-IR and LAR, both suggest that inhibition of IL-6 signalling in human subjects with rheumatoid diseases improves insulin sensitivity. Since 2001 several population based studies have shown a positive correlation of IL-6 serum levels and insulin resistance in human subjects. However, the association of IL-6 and type 2 diabetes is not well understood to date, as several studies in rodents and humans have reported contradictory results.