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Key molecule identified in the origin of insulin resistance

(Vienna, 16 Feb. 2010) The young scientist Dr. Florian Kiefer from the Medical University of Vienna has been able to identify a key factor in the origin of type 2 diabetes. It has been discovered that the protein "osteopontin" is a key molecule in the inflammation associated with obesity which leads to insulin resistance. The publication was made in the internationally renowned specialist journal "Diabetes".

90 percent of type 2 diabetes patients are overweight. There is a clear connection between obesity and suffering from type 2 diabetes, but the mechanisms behind this have not been studied enough. Obesity leads to a weak but chronic inflammatory response, which impairs the effect of insulin and is a decisive factor in leading to type 2 diabetes. The inflammation with obesity is characterised by an increase in circulating inflammation markers such as "C-reactive protein" and "tumour necrosis factor α". The cause of this inflammatory response is the fatty tissue in which inflammatory cells migrate and produce messenger substances there, which means that the inflammatory response also affects other organs.

New treatment strategy for type 2 diabetes?
In a previous study, Kiefer and his colleagues from the working group of Univ. Prof. Dr. Thomas Stulnig at the Division of Endocrinology and Metabolism in Department of Medicine III were able to show that the inflammatory protein osteopontin is dramatically upregulated in the fatty tissue with obesity and is produced almost entirely from inflammatory macrophages used to remove foreign matter. In the now published work, the researchers from the working group have managed to neutralise the effect of osteopontin with an antibody in obese mice. This meant that not only was the inflammation of the fatty tissue drastically reduced, the insulin effect was also significantly improved. With diabetes patients the impaired effect of insulin in the liver plays a decisive role in the increased fasting blood sugar levels. With the neutralisation of osteopontin, the glucose metabolism in obese mice was able to be largely normalised. The inhibition of osteopontin could therefore represent a new strategy for the treatment of complications with obesity such as type 2 diabetes.

About the author
Florian Kiefer studied medicine in Vienna and Heidelberg and completed scientific studies at the Medical University of Vienna with the PhD programme »Cell Communication in Health and Disease – CCHD« in the working group of Univ. Prof. Dr. Thomas Stulnig (Division of Endocrinology and Metabolism, Department of Medicine III). Dr. Kiefer has currently interrupted his specialist training for a two-year research stay at Brigham and Women’s Hospital, Harvard University, Boston, MA, USA.

» Original Publication
Florian W. Kiefer, MD, Maximilian Zeyda, PhD, Karina Gollinger, Birgit Pfau, Angelika Neuhofer, Thomas Weichhart, PhD, Marcus D. Säemann, MD, René Geyeregger, PhD, Michaela Schlederer, Lukas Kenner, MD, and Thomas M. Stulnig, MD. Neutralization of osteopontin inhibits obesity-induced inflammation and insulin resistance. Diabetes. 2010