Abstract
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 β‐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 β‐cell dysfunction, hypothalamic control of energy balance, and the pathogenesis of T2DM and obesity.
Original language | English |
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Article number | 1900934 |
Number of pages | 11 |
Journal | Molecular Nutrition & Food Research |
Volume | 65 |
Issue number | 1 |
Early online date | 20 Apr 2020 |
DOIs | |
Publication status | Published - Jan 2021 |
Bibliographical note
Open Access via the Wiley Jisc DealFunded by:
Rural and Environment Science and Analytical Services Division
Commonwealth Scientific and Industrial Research Organisation (CSIRO; Australia)
Keywords
- Western diet
- advanced glycation end products
- inflammation
- metabolic dysfunction
- processed foods
- OXIDATIVE STRESS
- CARBOXYMETHYL-LYSINE
- TRANSEPITHELIAL FLUX
- ENDPRODUCTS AGES
- DIABETES-MELLITUS
- SKELETAL-MUSCLE
- INSULIN-RESISTANCE
- CACO-2 CELL MONOLAYERS
- POTENTIAL ROLE
- TRANSGENIC MICE