國家衛生研究院 NHRI:Item 3990099045/10634
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    题名: Hyperglycemia and advanced glycation end products (AGEs) suppress the differentiation of 3T3-L1 preadipocytes
    作者: Chang, CC;Chen, CY;Chang, GD;Chen, TH;Chen, WL;Wen, HC;Huang, CY;Chang, CH
    贡献者: Institute of Cellular and Systems Medicine
    摘要: 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 PPARgamma and C/EBPalpha. Levels or activities of Src, PDK1, Akt, and NF-kappaB 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-kappaB. 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-kappaB pathway and impair adipogenesis.
    日期: 2017-08
    關聯: Oncotarget. 2017 Aug;8(33):55039-55050.
    Link to: http://dx.doi.org/10.18632/oncotarget.18993
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000407826100091
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85029085760
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