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Am J Clin Nutr. 2016 Jun;103(6):1426-33. doi: 10.3945/ajcn.115.125427. Epub 2016 Mar 30.

Diet low in advanced glycation end products increases insulin sensitivity in healthy overweight individuals: a double-blind, randomized, crossover trial.

Author information

1
Monash Centre for Health, Research and Implementation, School of Public Health and Preventive Medicine, and Baker IDI Heart and Diabetes Institute, Melbourne, Australia; barbora.decourten@monash.edu josephine.forbes@mater.uq.edu.au.
2
Centre for Chronic Disease, College of Health and Biomedicine, Victoria University, Melbourne, Australia;
3
Monash Centre for Health, Research and Implementation, School of Public Health and Preventive Medicine, and Baker IDI Heart and Diabetes Institute, Melbourne, Australia;
4
Baker IDI Heart and Diabetes Institute, Melbourne, Australia;
5
Laboratory for Metabolism and Vascular Medicine, Experimental Internal Medicine, Maastricht University, Maastricht, Netherlands;
6
Department of Nutrition and Dietetics, Monash University, Melbourne, Australia; Baker IDI Heart and Diabetes Institute, Melbourne, Australia;
7
Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Glycation and Diabetes, Mater Research Institute-University of Queensland, ITranslational Research Institute, Brisbane, Australia; and Mater Clinical School, University of Queensland, Brisbane, Australia barbora.decourten@monash.edu josephine.forbes@mater.uq.edu.au.

Abstract

BACKGROUND:

The consumption of advanced glycation end products (AGEs) has increased because of modern food processing and has been linked to the development of type 2 diabetes in rodents.

OBJECTIVE:

We determined whether changing dietary AGE intake could modulate insulin sensitivity and secretion in healthy, overweight individuals.

DESIGN:

We performed a double-blind, randomized, crossover trial of diets in 20 participants [6 women and 14 men; mean ± SD body mass index (in kg/m(2)): 29.8 ± 3.7]. Isoenergetic- and macronutrient-matched diets that were high or low in AGE content were alternately consumed for 2 wk and separated by a 4-wk washout period. At the beginning and end of each dietary period, a hyperinsulinemic-euglycemic clamp and an intravenous glucose tolerance test were performed. Dietary, plasma and urinary AGEs N(€)-(carboxymethyl)lysine (CML), N(€)-(carboxyethyl)lysin (CEL), and methylglyoxal-derived hydroimadazolidine (MG-H1) were measured with the use of mass spectrometry.

RESULTS:

Participants consumed less CML, CEL, and MG-H1 during the low-AGE dietary period than during the high-AGE period (all P < 0.05), which was confirmed by changes in urinary AGE excretion. There was an overall difference in insulin sensitivity of -2.1 mg · kg(-1) · min(-1) between diets (P = 0.001). Insulin sensitivity increased by 1.3 mg · kg(-1) · min(-1) after the low-AGE diet (P = 0.004), whereas it showed a tendency to decrease by 0.8 mg · kg(-1) · min(-1) after the high-AGE diet (P = 0.086). There was no difference in body weight or insulin secretion between diets (P = NS).

CONCLUSIONS:

A diet that is low in AGEs may reduce the risk of type 2 diabetes by increasing insulin sensitivity. Hence, a restriction in dietary AGE content may be an effective strategy to decrease diabetes and cardiovascular disease risks in overweight individuals. This trial was registered at clinicaltrials.gov as NCT00422253.

KEYWORDS:

glycotoxin; insulin resistance; insulin secretion; obesity; receptors for AGEs

Comment in

PMID:
27030534
DOI:
10.3945/ajcn.115.125427
[Indexed for MEDLINE]

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