title: Possible link of food-derived advanced glycation end products (AGEs) to the development of diabetes.
abstract: China Da Qing diabetes prevention study has recently shown that group-based lifestyle interventions over six years can prevent or delay the development of diabetes in patients with impaired glucose tolerance (IGT) for up to 14 years after the active intervention. These findings suggest the sustained beneficial effects of lifestyle interventions to prevent diabetes in at-risk patients for diabetes. Therefore, the clinical study suggests that so-called 'metabolic memory' is involved in the development of diabetes. Potential mechanisms for propagating this 'metabolic memory' are the non-enzymatic glycation of proteins. The formation and accumulation of advanced glycation end products (AGEs) have been known to progress at an accelerated rate under diabetes, and there is accumulating evidence that AGEs play a role in the development of diabetes by inducing islet beta cell damage and/or insulin resistance. Further, there are several animal studies to suggest that dietary AGEs are involved in insulin resistance, visceral obesity and the development of diabetes. These findings led us to speculate that the long-term beneficial influence of early lifestyle interventions on the development of diabetes could be ascribed, at least in part, to their inhibitory effects on AGEs. That is, intake of food-derived AGEs may be suppressed in the lifestyle intervention group, which could reduce the risk for the development of diabetes in high-risk patients with IGT. Therefore, it is an interesting issue to clarify whether food-derived AGEs are actually restricted during the active intervention period and if circulating or tissue AGE levels at the closure of the China Da Qing diabetes prevention study could predict the risk for the development of diabetes 14 years after the trial. This additional, clinical investigation may provide us more information about whether restriction of food-derived AGEs is beneficial for the prevention of the development of diabetes in high-risk patients and may be a novel therapeutic target to prevent diabetes and its related complications.
authors.affiliation: Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume 830-0011, Japan. schoichi@med.kurume-u.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Yamagishi
authors.forename: T
authors.initials: T
authors.lastname: Matsui
authors.forename: K
authors.initials: K
authors.lastname: Nakamura
mesh_terms: D003920:Diabetes Mellitus / Q000139:chemically induced* / Q000517:prevention & control*; D004032:Diet; D005504:Food Analysis; D017127:Glycation End Products, Advanced / Q000009:adverse effects*; D006801:Humans; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000502:physiology; D009765:Obesity / Q000139:chemically induced
chemical_list: D017127:Glycation End Products, Advanced