PMID- 32246887
OWN - NLM
STAT- MEDLINE
DCOM- 20210927
LR  - 20210927
IS  - 1613-4133 (Electronic)
IS  - 1613-4125 (Linking)
VI  - 65
IP  - 1
DP  - 2021 Jan
TI  - The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction.
PG  - e1900934
LID - 10.1002/mnfr.201900934 [doi]
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 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.
CI  - (c) 2020 The Authors. Molecular Nutrition & Food Research published by Wiley-VCH 
      Verlag GmbH & Co. KGaA.
FAU - Sergi, Domenico
AU  - Sergi D
AD  - Nutrition and Health Substantiation Group, Nutrition and Health Program, Health 
      and Biosecurity, Commonwealth Scientific and Industrial Research Organisation 
      (CSIRO), Adelaide, SA, 5000, Australia.
AD  - Adelaide Medical School, The University of Adelaide, Adelaide, SA, 5000, 
      Australia.
FAU - Boulestin, Hakim
AU  - Boulestin H
AD  - Rowett Institute, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
FAU - Campbell, Fiona M
AU  - Campbell FM
AD  - Rowett Institute, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
FAU - Williams, Lynda M
AU  - Williams LM
AD  - Rowett Institute, University of Aberdeen, Aberdeen, AB25 2ZD, UK.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20200420
PL  - Germany
TA  - Mol Nutr Food Res
JT  - Molecular nutrition & food research
JID - 101231818
RN  - 0 (Antigens, Neoplasm)
RN  - 0 (Enzymes)
RN  - 0 (Glycation End Products, Advanced)
RN  - EC 2.7.11.22 (MOK protein, human)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Antigens, Neoplasm/metabolism
MH  - Cooking
MH  - Diabetes Mellitus, Type 2/*metabolism
MH  - Diet
MH  - Diet, Western/adverse effects
MH  - Enzymes/*metabolism
MH  - Glycation End Products, Advanced/*metabolism
MH  - Humans
MH  - Inflammation/etiology
MH  - Insulin-Secreting Cells/metabolism
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - Obesity/etiology/*metabolism
OTO - NOTNLM
OT  - Western diet
OT  - advanced glycation end products
OT  - inflammation
OT  - metabolic dysfunction
OT  - processed foods
EDAT- 2020/04/05 06:00
MHDA- 2021/09/28 06:00
CRDT- 2020/04/05 06:00
PHST- 2019/12/02 00:00 [received]
PHST- 2020/03/09 00:00 [revised]
PHST- 2020/04/05 06:00 [pubmed]
PHST- 2021/09/28 06:00 [medline]
PHST- 2020/04/05 06:00 [entrez]
AID - 10.1002/mnfr.201900934 [doi]
PST - ppublish
SO  - Mol Nutr Food Res. 2021 Jan;65(1):e1900934. doi: 10.1002/mnfr.201900934. Epub 
      2020 Apr 20.