title: Hypothesis: the 'metabolic memory', the new challenge of diabetes.
abstract: Large randomized studies have established that early intensive glycaemic control reduces the risk of diabetic complications, both micro- and macrovascular. However, epidemiological and prospective data support a long-term influence of early metabolic control on clinical outcomes. This phenomenon has recently been defined as 'metabolic memory.' Potential mechanisms for propagating this 'memory' are the non-enzymatic glycation of cellular proteins and lipids, and an excess of cellular reactive oxygen and nitrogen species, in particular originated at the level of glycated-mitochondrial proteins, perhaps acting in concert with one another to maintain stress signalling. Furthermore, the emergence of this 'metabolic memory' suggests the need for very early aggressive treatment aiming to 'normalize' glycaemic control and the addition of agents which reduce cellular reactive species and glycation in order to minimize long-term diabetic complications.
authors.affiliation: Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK.
authors.forename: M A
authors.initials: MA
authors.lastname: Ihnat
authors.forename: J E
authors.initials: JE
authors.lastname: Thorpe
authors.forename: A
authors.initials: A
authors.lastname: Ceriello
mesh_terms: D000818:Animals; D001786:Blood Glucose; D048909:Diabetes Complications / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006031:Glycosylation; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000503:physiopathology*; D008928:Mitochondria / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats
chemical_list: D001786:Blood Glucose; D017127:Glycation End Products, Advanced; D009569:Nitric Oxide