title: Elevated serum advanced glycation endproducts in obese indicate risk for the metabolic syndrome: a link between healthy and unhealthy obesity?
abstract: BACKGROUND
  Although obesity can predispose to the metabolic syndrome (MS), diabetes, and cardiovascular disease, not all obese subjects develop MS, hence the need for new indicators of risk for this syndrome. Advanced glycation end products (AGEs) correlate with factors involved in the MS, including inflammation and insulin resistance (IR). Because AGEs can be derived from food and are modifiable, it is important to determine whether they are a risk factor for MS.
  
  
  OBJECTIVE
  The objective of this study was to assess the association of endogenous and exogenous AGEs with MS criteria.
  
  
  METHODS
  The following data were collected in a cross-sectional study of subjects with and without the MS: serum AGEs (sAGEs) and mononuclear cell AGEs, metabolites, pro- and antiinflammatory markers, body fat mass measures, including abdominal magnetic resonance imaging, and caloric and dietary AGE (dAGE) consumption.
  
  
  METHODS
  The study was conducted in the general community.
  
  
  METHODS
  Participants included 130 MS and 139 non-MS subjects of both sexes, older than 50 years.
  
  
  RESULTS
  sAGEs ((ϵ)N-carboxymethyllysine, methylglyoxal) were markedly elevated in obese persons with more than one other MS criteria but not in obese without MS criteria. sAGEs directly correlated with markers of IR (HOMA) and inflammation (leptin, TNFα, RAGE) and inversely with innate defenses (SIRT1, AGE receptor 1 [AGER1], glyoxalase-I, adiponectin). sAGEs correlated with dAGEs but not with calories, nutrient consumption, or fat mass measures. Consumption of dAGE, but not of calories, was markedly higher in MS than in non-MS.
  
  
  CONCLUSIONS
  High sAGEs, a modifiable risk factor for IR, may indicate risk for the MS, type 2 diabetes, and cardiovascular disease. High dietary AGE consumption and serum AGE levels may link healthy obesity to at-risk obesity.
authors.affiliation: Department of Geriatrics, Division of Experimental Diabetes (W.C., E.T., L.G., R.P., K.Y., L.T., X.C., H.V.), Department of Medicine, Division of Nephrology (J.U., H.V.), and Translational and Molecular Imaging Institute (V.M., Z.A.F.), The Icahn School of Medicine at Mt Sinai, New York, New York 10029; and George Institute for Global Health (M.W.), University of Oxford, Oxford OX1 3QX, United Kingdom, and University of Sydney, Sydney 2006, Australia.
authors.forename: Jaime
authors.initials: J
authors.lastname: Uribarri
authors.forename: Weijing
authors.initials: W
authors.lastname: Cai
authors.forename: Mark
authors.initials: M
authors.lastname: Woodward
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Tripp
authors.forename: Laurie
authors.initials: L
authors.lastname: Goldberg
authors.forename: Renata
authors.initials: R
authors.lastname: Pyzik
authors.forename: Kalle
authors.initials: K
authors.lastname: Yee
authors.forename: Laurie
authors.initials: L
authors.lastname: Tansman
authors.forename: Xue
authors.initials: X
authors.lastname: Chen
authors.forename: Venkatesh
authors.initials: V
authors.lastname: Mani
authors.forename: Zahi A
authors.initials: ZA
authors.lastname: Fayad
authors.forename: Helen
authors.initials: H
authors.lastname: Vlassara
mesh_terms: D000368:Aged; D003430:Cross-Sectional Studies; D005260:Female; D017127:Glycation End Products, Advanced / Q000097:blood*; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000209:etiology; D008875:Middle Aged; D009765:Obesity / Q000097:blood* / Q000150:complications; D012307:Risk Factors
chemical_list: D017127:Glycation End Products, Advanced