Context: While obesity can predispose to the metabolic syndrome (MS), diabetes (T2D) and cardiovascular disease (CVD), not all obese subjects develop MS, hence the need for new indicators of risk for this syndrome. Advanced glycation endproducts (AGEs) correlate with factors involved in the MS, including inflammation and insulin resistance (IR). Since AGEs can be derived from food and are modifiable, it is important to determine if they are a risk factor for MS. Objective: To assess the association of endogenous and exogenous AGEs with MS criteria. Design: The following data were collected in a cross-sectional study of subjects with and without the MS: serum AGEs (sAGEs) and mononuclear cell AGEs (iAGEs), metabolites, pro- and anti-inflammatory markers, body fat mass measures, including abdominal MRI, caloric and dietary AGE (dAGE) consumption. Setting: General community. Participants: 130 MS and 139 non-MS subjects of both sexes, >50 years old. Results: sAGEs(CML, MG) were markedly elevated in obese persons with >1 other MS criteria but not in obese without MS criteria. sAGEs directly correlated with markers of IR and inflammation (HOMA, leptin, TNFalpha, RAGE) and inversely with innate defenses (SIRT1, AGER1, Glyoxalase-I, Adiponectin). sAGEs correlated with dAGEs but not with calories, nutrient consumption, or fat mass measures. Consumption of dAGEs, but not of calories, was markedly higher in MS than in non-MS. Conclusion: High sAGEs, a modifiable risk factor for IR, may indicate persons at-risk for the MS, T2D and CVD. High dietary AGE consumption and serum AGE levels may link healthy obesity to at-risk obesity.
a1945-7197 (Electronic)