Oncotarget

Research Papers:

Hyperglycemia and advanced glycation end products (AGEs) suppress the differentiation of 3T3-L1 preadipocytes

Chia-Chu Chang, Chen-Yu Chen, Geen-Dong Chang, Ting-Huan Chen, Woan-Ling Chen, Hui-Chin Wen, Chih-Yang Huang and Chung-Ho Chang _

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Oncotarget. 2017; 8:55039-55050. https://doi.org/10.18632/oncotarget.18993

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Abstract

Chia-Chu Chang1,2,3,*, Chen-Yu Chen4,*, Geen-Dong Chang5, Ting-Huan Chen3,4,6, Woan-Ling Chen3,7, Hui-Chin Wen1, Chih-Yang Huang1 and Chung-Ho Chang1,3,4

1Graduate Institute of Basic Medical Science, Ph.D. Program for Aging, China Medical University, Taichung, Taiwan 40402, Republic of China

2School of Medicine, Chung Shan Medical University, Taichung, Taiwan 40201, Republic of China

3Environmental and Precision Medicine Laboratory, Department of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan 50006, Republic of China

4Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Miaoli, Taiwan 35053, Republic of China

5Graduate Institute of Biochemical Sciences, School of Life Science, National Taiwan University, Taipei, Taiwan 10617, Republic of China

6Department of Life Science, National Tsing Hua University, Hsinchu, Taiwan 30013, Republic of China

7Department of Food Science, Tunghai University, Taichung, Taiwan 40704, Republic of China

*These authors contributed equally to this work

Correspondence to:

Chung-Ho Chang, email: [email protected]

Keywords: advanced glycation end products (AGEs), hyperglycemia, adipogenesis, NF-kB, Bcl-2

Received: December 28, 2016     Accepted: June 18, 2017     Published: July 05, 2017

ABSTRACT

Aging is characterized by mild hyperglycemia and accumulation of advanced glycation end products (AGEs). Effects of chronic exposure to hyperglycemia or AGEs on the adipogenic differentiation of 3T3-L1 preadipocytes remain unclear. We examined the chronic effect of AGEs and high glucose on the differentiation of 3T3-L1 cells by culturing 3T3-L1 cells in the presence of AGEs or 25 mM glucose for 1 month. Chronic incubation of 3T3-L1 cells with AGEs or high glucose blocked their differentiation into mature adipocytes as evidenced by reduced levels of adipocyte markers such as accumulated oil droplets, GPDH, aP2, adiponectin and of adipogenesis regulators PPARγ and C/EBPα. Levels or activities of Src, PDK1, Akt, and NF-κB were higher in AGEs- and high glucose-treated cells than those in 3T3-L1 cells. Levels of Bcl-2 were elevated in AGEs- and high glucose-treated cells, and were attenuated by inhibitors of PI3-kinase, Akt and NF-κB. Moreover, adipogenesis was attenuated in 3T3-L1 cells stably expressing Bcl-2 or YAP. These results suggest that chronic AGEs and high glucose treatments up-regulate Bcl-2 and YAP via the Akt-NF-κB pathway and impair adipogenesis.


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