TY - JOUR
T1 - The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction
AU - Sergi, Domenico
AU - Boulestin, Hakim
AU - Campbell, Fiona M
AU - Williams, Lynda M
N1 - Open Access via the Wiley Jisc Deal
Funded by:
Rural and Environment Science and Analytical Services Division
Commonwealth Scientific and Industrial Research Organisation (CSIRO; Australia)
PY - 2021/1
Y1 - 2021/1
N2 - 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.
AB - 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.
KW - Western diet
KW - advanced glycation end products
KW - inflammation
KW - metabolic dysfunction
KW - processed foods
KW - OXIDATIVE STRESS
KW - CARBOXYMETHYL-LYSINE
KW - TRANSEPITHELIAL FLUX
KW - ENDPRODUCTS AGES
KW - DIABETES-MELLITUS
KW - SKELETAL-MUSCLE
KW - INSULIN-RESISTANCE
KW - CACO-2 CELL MONOLAYERS
KW - POTENTIAL ROLE
KW - TRANSGENIC MICE
UR - http://www.scopus.com/inward/record.url?scp=85083669549&partnerID=8YFLogxK
U2 - 10.1002/mnfr.201900934
DO - 10.1002/mnfr.201900934
M3 - Review article
C2 - 32246887
VL - 65
JO - Molecular Nutrition & Food Research
JF - Molecular Nutrition & Food Research
SN - 1613-4125
IS - 1
M1 - 1900934
ER -