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The Pro‐Adipogenic Effect of Advanced Glycation End‐Products (AGEs) in Adipogenesis
Author(s) -
Chen Chih yu,
Martorano Allison,
Kim KeeHong
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.547.7
Subject(s) - adipogenesis , glycation , rage (emotion) , methylglyoxal , obesity , endocrinology , inflammation , medicine , endogeny , oxidative stress , receptor , adipose tissue , advanced glycation end product , chemistry , biology , biochemistry , neuroscience , enzyme
Obesity is a public health problem in the United States and globally. Adipogenesis plays a critical role in regulation between obesity and metabolic failure diseases. Advanced glycation end‐products (AGEs), through its receptor (RAGE), are known to induce oxidative stress, inflammation, and aging‐related chronic diseases including diabetes and cardiovascular disease. The inhibition of the AGE‐RAGE interaction has been proposed as a target for treatment and prevent of these diseases, however little is known about the effect in obesity. The objective of this study was to determine the role of AGE during adipogenesis of 3T3‐L1 cells. We found that adipogenesis is associated with induction of endogenous AGE and RAGE mRNA. We also observed that the passage number of 3T3‐L1 cells directly affected the cellular levels of endogenous AGE, RAGE mRNA expression and oxidative stress. Using bovine serum albumin glycated with methylglyoxal as an in vitro model of AGE, we revealed that exogenous AGE increased adipogenesis and the mRNA level of RAGE. The pro‐adipogenic effect of AGE was more effective to higher passage number cells. These results suggest that AGE function and/or the AGE‐ RAGE axis might play a critical role in augmenting the development of adipose tissue. This project is partially funded by USDA‐AFRI grant and The Showalter Trust Fund Award. Grant Funding Source : USDA‐AFRI and The Showalter Trust Fund Award