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Submitted on August 19, 2008
Accepted on November 25, 2008
Warwick Medical School, University of Warwick, U.K.; and INRCA, Diabetes Unit, Ancona – Italy; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
* To whom correspondence should be addressed. E-mail: antonio.ceriello{at}warwick.ac.uk.
Context. The concept of a "metabolic memory," that is of diabetic vascular stresses persisting after glucose normalization, has been supported both in the laboratory and in the clinic and in both type 1 and type 2 diabetes.
Evidence acquisition. Using PubMed, we searched for publications on diabetic micro- and macrovascular complications using terms such as persistence, prolongation, sustained, and "memory" and focusing on the mechanistic basis behind this "metabolic memory."
Evidence synthesis. We found that as early as the mid-1980s this "memory" phenomenon was described in diabetic animals and isolated cells exposed to high glucose followed by normalized glucose and then beginning around 2002 in results from large clinical trials such as the DCCT-EDIC and the UKPDS. Further, mechanisms for propagating this "memory" appear focused on the nonenzymatic glycation of cellular proteins and lipids and on an excess of cellular reactive oxygen and nitrogen species, in particular originating at the level of glycated mitochondrial proteins and perhaps acting in concert with one another to maintain stress signaling independent of glucose levels.
Conclusions. The emergence of this "Metabolic Memory" suggests the need of early aggressive treatment aiming to "normalize" metabolic control together perhaps with the addition of agents which reduce cellular reactive species and glycation in order to minimize long-term diabetic complications.
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