4.7 Review

The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction

Journal

MOLECULAR NUTRITION & FOOD RESEARCH
Volume 65, Issue 1, Pages -

Publisher

WILEY
DOI: 10.1002/mnfr.201900934

Keywords

advanced glycation end products; inflammation; metabolic dysfunction; processed foods; Western diet

Funding

  1. Scottish Government's Rural and Environment Science and Analytical Services Division (RESAS)
  2. Commonwealth Scientific and Industrial Research Organisation (CSIRO
  3. Australia) Postdoctoral Research Fellowship

Ask authors/readers for more resources

AGEs are a group of molecules produced through non-enzymatic reactions, implicated in complications of diabetes and metabolic health, contributing to the development of type 2 diabetes and obesity.
Advanced glycation end products (AGEs) are a heterogeneous group of molecules produced, non-enzymatically, from the interaction between reducing sugars and the free amino groups of proteins, nucleic acids, and lipids. AGEs are formed as a normal consequence of metabolism but can also be absorbed from the diet. They have been widely implicated in the complications of diabetes affecting cardiovascular health, the nervous system, eyes, and kidneys. Increased levels of AGEs are also detrimental to metabolic health and may contribute to the metabolic abnormalities induced by the Western diet, which is high in processed foods and represents a significant source of AGEs. While increased AGE levels are a consequence of diabetic hyperglycaemia, AGEs themselves activate signaling pathways, which compromise insulin signaling and pancreatic beta-cell function, thus, contributing to the development of type 2 diabetes mellitus (T2DM). Furthermore, AGEs may also contribute to the obesogenic effects of the Western diet by promoting hypothalamic inflammation and disrupting the central control of energy balance. Here, the role of dietary AGEs in metabolic dysfunction is reviewed with a focus on the mechanisms underpinning their detrimental role in insulin resistance, pancreatic beta-cell dysfunction, hypothalamic control of energy balance, and the pathogenesis of T2DM and obesity.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available