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Effect of dietary advanced glycation end products on postprandial appetite, inflammation, and endothelial activation in healthy overweight individuals

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Abstract

Purpose

Advanced glycation end products (AGEs) formed in food during high-heat cooking may induce overeating and inflammation. We investigated whether AGE contents in a single meal affect postprandial appetite and markers of inflammation, endothelial activation, and oxidative stress.

Methods

In total, 19 healthy overweight individuals completed a crossover meal test with two meals of identical ingredients prepared by roasting (H-AGE) or steaming (L-AGE), respectively. Postprandial blood samples were analysed for Nε-carboxymethyl-lysine (CML), appetite-regulating gut hormones, glucose, insulin, triacylglycerol, and markers of inflammation and endothelial activation. Subjective appetite ratings and subsequent food intake were also assessed, and urine was analysed for CML, methylglyoxal-derived hydroimidazolone (MG-H1), and F2-isoprostanes.

Results

CML content of the H- and L-AGE meals was 5.0 and 2.8 mg, respectively. Plasma CML and urinary CML and MG-H1 tended to be higher after the H-AGE meal. There was no change in subsequent food intake, appetite sensations, or appetite hormone responses between meals, except for the overall ghrelin response, which was higher after the H-AGE meal compared with the L-AGE meal (p = 0.016). There was an increased glycaemic response to the H-AGE meal (p = 0.027) compared with the L-AGE meal. Inflammatory and endothelial activation markers did not differ between meals, but there was an overall effect on endothelial activation (p = 0.021) and on the oxidative marker, F2-isoprostanes, in urine (p = 0.013).

Conclusion

The present study did not show any pronounced effects of AGEs on appetite and markers of inflammation, but did indicate that AGEs may affect postprandial ghrelin, oxidative stress, and glucose responses.

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Abbreviations

AGE:

Advanced glycation end product

AUC:

Area under curve

CML:

Nε-carboxymethyl-lysine

CRP:

C-reactive protein

GLP-1:

Glucagon-like peptide-1

H-AGE:

High-advanced glycation end products

ICAM-1:

Intercellular adhesion molecule-1

IL-6:

Interleukin-6

L-AGE:

Low-advanced glycation end product

MG-H1:

Methylglyoxal-derived hydroimidazolone

PABA:

Para-aminobenzoic acid

PYY:

Peptide YY

RAGE:

Receptor for advanced glycation end product

TNF-α:

Tumour necrosis factor-α

VAS:

Visual analogue scale

VCAM-1:

Vascular cell adhesion molecule-1

isoPGF :

F2-isoprostaglandins

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Acknowledgments

The authors would like to thank Pia Lisbeth Madsen, Hanne Lysdal Petersen, Sarah Fleischer Ben Soltane, Charlotte Kostecki, and Yvonne Fatum for their excellent technical assistance, students Anne-Ditte Termannsen and Pia Øllgaard Olsen for their assistance with data collection, and the volunteers who participated in the study. The work was carried out as part of the research programme of the UNIK: Food, Fitness & Pharma for Health and Disease (see www.footfitnesspharma.ku.dk). The UNIK project is supported by the Danish Ministry of Science, Technology and Innovation. Additional samples for collaboration are stored in the open biobank CUBE (www.cube.ku.dk). The authors declare no conflicts of interest. MWP, LL, SB, and LOD designed the study. MWP and ACG-F conducted the study. MJB and JJH carried out the analyses of gut hormones. JMA and JN synthesised standards for the AGE analysis. JMA carried out the analysis of AGEs. RM carried out the analysis of isoprostanes. MWP performed the statistical analyses and wrote the manuscript. LHL, LL, SB, and LOD provided significant scientific advice on the interpretation of the data. All authors revised and approved the final manuscript.

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Correspondence to Lars O. Dragsted.

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The study was registered at www.clinicaltrials.gov with identifier NCT01434407.

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Poulsen, M.W., Bak, M.J., Andersen, J.M. et al. Effect of dietary advanced glycation end products on postprandial appetite, inflammation, and endothelial activation in healthy overweight individuals. Eur J Nutr 53, 661–672 (2014). https://doi.org/10.1007/s00394-013-0574-y

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  • DOI: https://doi.org/10.1007/s00394-013-0574-y

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