Journal
ONCOTARGET
Volume 8, Issue 33, Pages 55039-55050Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.18993
Keywords
advanced glycation end products (AGEs); hyperglycemia; adipogenesis; NF-kappa B; Bcl-2
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Funding
- Ministry of Science and Technology [MOST 104-2320-B-400-008, 105-2314-B-371-005]
- National Health Research Institutes [CS-PP03]
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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 PPAR. and C/EBPa. Levels or activities of Src, PDK1, Akt, and NF-kappa B 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-kappa B. 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-kappa B pathway and impair adipogenesis.
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