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

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.

Nonword reading and Stroop interference: what differentiates attention-deficit/hyperactivity disorder and reading disability?

BACKGROUND: Attention deficits and impaired reading performance co-occur more often than expected by chance; however, the underlying mechanism of this association still remains rather unexplored. METHOD: In two consecutive studies, children aged 8 to 12 years with attention-deficit/hyperactivity disorder (ADHD) and children with reading disability (RD) were examined using a 2 (ADHD versus no ADHD) × 2 (RD versus no RD) factorial design. To further delineate deficient interference control from reading processes, we used a newly developed self-paced word/nonword reading task (Experiment 1, n = 68) and a modified computerized Stroop paradigm, including an orthographic phonological neighbor (OPN) condition (Experiment 2, n = 84). RESULTS: RD (compared to non-RD groups) was associated with impairments in both word and nonword reading, while children with ADHD also showed impaired nonword reading. In the Stroop task, RD, but not ADHD, had a significant impact on task performance. Interestingly, a significant interaction between ADHD, RD, and task condition emerged, which was due to particularly slower reaction times to nonwords in children with RD only, while task performance in children with comorbid ADHD and RD resembled that of ADHD only. CONCLUSIONS: Thus, our results demonstrate that impairments in nonword reading were not specific to RD but were also present in children with ADHD. In addition, RD and not ADHD was characterized by poor interference control in the Stroop task. These findings question whether unique cognitive deficits are specific to either ADHD or RD.