Inhibition of advanced glycation endproduct formation by foodstuffs

Chi Hao Wu, Shang Ming Huang, Jer An Lin, Gow Chin Yen

Research output: Contribution to journalArticle

176 Citations (Scopus)

Abstract

The Maillard reaction, which is generally termed nonenzymatic browning or glycation, has been implicated in accelerated aging and diabetic complications in vivo. Although the molecular basis of glycation-induced pathogenesis is not well understood, the following have been noted: (1) protein glycation leads to the formation and accumulation of toxic advanced glycation endproducts (AGEs); (2) AGEs can permanently alter the structure and function of body proteins; and (3) the interaction between AGE-modified proteins and AGE-specific receptors (RAGEs) on the cell surface induces the overproduction of reactive oxygen species (ROSs) and inflammatory mediators, which leads to cellular disorders in biological systems. To date, studies that have examined the contribution of protein glycation to disease-states have primarily focused on the deleterious effects and related mechanisms of these glycotoxins. However, it remains unknown whether phytochemicals exert protective effects against glycotoxin-induced damage. Thus, the development and investigation of AGE inhibitors, especially the natural anti-AGE agents without adverse effects, may provide a therapeutic approach for delaying and preventing premature aging and diabetic complications. In this review, we provide an outline of anti-glycation properties of foodstuffs and/or their active components, and discuss their mechanisms of action.

Original languageEnglish
Pages (from-to)224-234
Number of pages11
JournalFood and Function
Volume2
Issue number5
DOIs
Publication statusPublished - May 2011
Externally publishedYes

Fingerprint

glycation
Diabetes Complications
Proteins
Maillard reaction
Premature Aging
Maillard Reaction
Poisons
Phytochemicals
Reactive Oxygen Species
proteins
body protein
phytopharmaceuticals
protective effect
advanced glycation end products
reactive oxygen species
mechanism of action
pathogenesis
adverse effects
therapeutics
receptors

ASJC Scopus subject areas

  • Food Science
  • Medicine(all)

Cite this

Inhibition of advanced glycation endproduct formation by foodstuffs. / Wu, Chi Hao; Huang, Shang Ming; Lin, Jer An; Yen, Gow Chin.

In: Food and Function, Vol. 2, No. 5, 05.2011, p. 224-234.

Research output: Contribution to journalArticle

Wu, Chi Hao ; Huang, Shang Ming ; Lin, Jer An ; Yen, Gow Chin. / Inhibition of advanced glycation endproduct formation by foodstuffs. In: Food and Function. 2011 ; Vol. 2, No. 5. pp. 224-234.
@article{9bfe2cecd6974fc6850a755b76b4f993,
title = "Inhibition of advanced glycation endproduct formation by foodstuffs",
abstract = "The Maillard reaction, which is generally termed nonenzymatic browning or glycation, has been implicated in accelerated aging and diabetic complications in vivo. Although the molecular basis of glycation-induced pathogenesis is not well understood, the following have been noted: (1) protein glycation leads to the formation and accumulation of toxic advanced glycation endproducts (AGEs); (2) AGEs can permanently alter the structure and function of body proteins; and (3) the interaction between AGE-modified proteins and AGE-specific receptors (RAGEs) on the cell surface induces the overproduction of reactive oxygen species (ROSs) and inflammatory mediators, which leads to cellular disorders in biological systems. To date, studies that have examined the contribution of protein glycation to disease-states have primarily focused on the deleterious effects and related mechanisms of these glycotoxins. However, it remains unknown whether phytochemicals exert protective effects against glycotoxin-induced damage. Thus, the development and investigation of AGE inhibitors, especially the natural anti-AGE agents without adverse effects, may provide a therapeutic approach for delaying and preventing premature aging and diabetic complications. In this review, we provide an outline of anti-glycation properties of foodstuffs and/or their active components, and discuss their mechanisms of action.",
author = "Wu, {Chi Hao} and Huang, {Shang Ming} and Lin, {Jer An} and Yen, {Gow Chin}",
year = "2011",
month = "5",
doi = "10.1039/c1fo10026b",
language = "English",
volume = "2",
pages = "224--234",
journal = "Food and Function",
issn = "2042-6496",
publisher = "Royal Society of Chemistry",
number = "5",

}

TY - JOUR

T1 - Inhibition of advanced glycation endproduct formation by foodstuffs

AU - Wu, Chi Hao

AU - Huang, Shang Ming

AU - Lin, Jer An

AU - Yen, Gow Chin

PY - 2011/5

Y1 - 2011/5

N2 - The Maillard reaction, which is generally termed nonenzymatic browning or glycation, has been implicated in accelerated aging and diabetic complications in vivo. Although the molecular basis of glycation-induced pathogenesis is not well understood, the following have been noted: (1) protein glycation leads to the formation and accumulation of toxic advanced glycation endproducts (AGEs); (2) AGEs can permanently alter the structure and function of body proteins; and (3) the interaction between AGE-modified proteins and AGE-specific receptors (RAGEs) on the cell surface induces the overproduction of reactive oxygen species (ROSs) and inflammatory mediators, which leads to cellular disorders in biological systems. To date, studies that have examined the contribution of protein glycation to disease-states have primarily focused on the deleterious effects and related mechanisms of these glycotoxins. However, it remains unknown whether phytochemicals exert protective effects against glycotoxin-induced damage. Thus, the development and investigation of AGE inhibitors, especially the natural anti-AGE agents without adverse effects, may provide a therapeutic approach for delaying and preventing premature aging and diabetic complications. In this review, we provide an outline of anti-glycation properties of foodstuffs and/or their active components, and discuss their mechanisms of action.

AB - The Maillard reaction, which is generally termed nonenzymatic browning or glycation, has been implicated in accelerated aging and diabetic complications in vivo. Although the molecular basis of glycation-induced pathogenesis is not well understood, the following have been noted: (1) protein glycation leads to the formation and accumulation of toxic advanced glycation endproducts (AGEs); (2) AGEs can permanently alter the structure and function of body proteins; and (3) the interaction between AGE-modified proteins and AGE-specific receptors (RAGEs) on the cell surface induces the overproduction of reactive oxygen species (ROSs) and inflammatory mediators, which leads to cellular disorders in biological systems. To date, studies that have examined the contribution of protein glycation to disease-states have primarily focused on the deleterious effects and related mechanisms of these glycotoxins. However, it remains unknown whether phytochemicals exert protective effects against glycotoxin-induced damage. Thus, the development and investigation of AGE inhibitors, especially the natural anti-AGE agents without adverse effects, may provide a therapeutic approach for delaying and preventing premature aging and diabetic complications. In this review, we provide an outline of anti-glycation properties of foodstuffs and/or their active components, and discuss their mechanisms of action.

UR - http://www.scopus.com/inward/record.url?scp=79957811092&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79957811092&partnerID=8YFLogxK

U2 - 10.1039/c1fo10026b

DO - 10.1039/c1fo10026b

M3 - Article

C2 - 21779560

AN - SCOPUS:79957811092

VL - 2

SP - 224

EP - 234

JO - Food and Function

JF - Food and Function

SN - 2042-6496

IS - 5

ER -