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Exp Clin Endocrinol Diabetes 2012; 120(04): 177-178
DOI: 10.1055/s-0032-1306299
Editorial
© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Innovative Models for Investigation of Pathomechanisms Leading to Late Diabetic Complications

P. Nawroth
1   Universitätsklinikum Heidelburg, Germany
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Publication Date:
23 April 2012 (online)

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Background

Recent studies have indicated that diabetes is a general term comprising several probably distinct disorders of metabolism, a term exceeding more than the difference between type 1 and type 2 diabetes [1]. Therefore it is not surprising that doubt has been raised, whether lowering glucose is the major and the only target goal, and whether glucose is the most important parameter for defining diabetes [1–5]. Recently studies have shown that posttranslational modification of the haemoglobin molecule predicts late complications even in patients with normal oral glucose tolerance, thus a subgroup of diabetics may exist in which diabetes is defined by complications rather than by glucose [6]. In view of several studies proving that normalization of blood pressure and optimal treatment of lipids is more effective than lowering glucose [7–9], it becomes now evident that innovative approaches for understanding late diabetic complications are needed. Furthermore it became obvious that glucose concentrations used in vitro to stimulate cells to mimic in vivo situations, are by far too high and may thus mislead the scientist, since in patients late diabetic complications do not occur primarily with glucose concentrations constantly above 200 mg/dl. Thus the question came up whether there are good animal models to unravel novel pathways and pave the way for treatment options different than lowering glucose, lipids or blood pressure.

 

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