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PLoS One. 2015 May 27;10(5):e0128293. doi: 10.1371/journal.pone.0128293. eCollection 2015.

Association between Advanced Glycation End Products and Impaired Fasting Glucose: Results from the SALIA Study.

Author information

1
Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Düsseldorf, Germany.
2
Institute of Food Chemistry, Technische Universität Dresden, Dresden, Germany.
3
IUF-Leibniz Research Institute for Environmental Medicine at Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
4
Department of Psychiatry and Psychotherapy, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
5
Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf, Düsseldorf, Germany; German Center for Diabetes Research (DZD e.V.), Partner Düsseldorf, Düsseldorf, Germany; Department of Endocrinology and Diabetology, Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
6
IUF-Leibniz Research Institute for Environmental Medicine at Heinrich Heine University Düsseldorf, Düsseldorf, Germany; Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
7
IUF-Leibniz Research Institute for Environmental Medicine at Heinrich Heine University Düsseldorf, Düsseldorf, Germany; Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland.

Abstract

Advanced glycation end products (AGEs) may contribute to the development of type 2 diabetes and related complications, whereas their role in the early deterioration of glycaemia is unknown. While previous studies used antibody-based methods to quantify AGEs, data from tandem mass spectrometry coupled liquid chromatography (LC-MS/MS)-based measurements are limited to patients with known diabetes. Here, we used the LC-MS/MS method to test the hypothesis that plasma AGE levels are higher in individuals with impaired fasting glucose (IFG) than in those with normal fasting glucose (NFG). Secondary aims were to assess correlations of plasma AGEs with quantitative markers of glucose metabolism and biomarkers of subclinical inflammation. This study included on 60 women with NFG or IFG (n = 30 each, mean age 74 years) from the German SALIA cohort. Plasma levels of free metabolites (3-deoxyfructose, 3-deoxypentosone, 3-deoxypentulose), two hydroimidazolones, oxidised adducts (carboxymethyllysine, carboxyethyllysine, methionine sulfoxide) and Nε-fructosyllysine were measured using LC-MS/MS. Plasma concentrations of all tested AGEs did not differ between the NFG and IFG groups (all p>0.05). Associations between plasma levels of AGEs and fasting glucose, insulin and HOMA-IR as a measure of insulin resistance were weak (r between -0.2 and 0.2, all p>0.05). The association between 3-deoxyglucosone-derived hydroimidazolone with several proinflammatory biomarkers disappeared upon adjustment for multiple testing. In conclusion, plasma AGEs assessed by LC-MS/MS were neither increased in IFG nor associated with parameters of glucose metabolism and subclinical inflammation in our study. Thus, these data argue against strong effects of AGEs in the early stages of deterioration of glucose metabolism.

PMID:
26018950
PMCID:
PMC4446029
DOI:
10.1371/journal.pone.0128293
[Indexed for MEDLINE]
Free PMC Article

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