Activation of AMP-Activated Protein Kinase Attenuates Tumor Necrosis Factor-α-Induced Lipolysis via Protection of Perilipin in 3T3-L1 Adipocytes
- Authors
- 홍석우[홍석우]; 이진미[이진미]; 박세은[박세은]; 이은정[이은정]; 박철영[박철영]; 오기원[오기원]; 박성우[박성우]; 이원영[이원영]
- Issue Date
- 2014
- Publisher
- 대한내분비학회
- Keywords
- AMP-activated protein kinases; Lipolysis; Perilipin; PERK/eIF2α; Adipocytes
- Citation
- Endocrinology and Metabolism, v.29, no.4, pp.553 - 560
- Indexed
- SCOPUS
KCI
- Journal Title
- Endocrinology and Metabolism
- Volume
- 29
- Number
- 4
- Start Page
- 553
- End Page
- 560
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/55016
- ISSN
- 2093-596X
- Abstract
- Background: Tumor necrosis factor (TNF)-α and AMP-activated protein kinase (AMPK) are known to stimulate and repress lipolysis in adipocytes, respectively; however, the mechanisms regulating these processes have not been completely elucidated.
Methods: The key factors and mechanism of action of TNF-α and AMPK in lipolysis were investigated by evaluating perilipin expression and activity of protein kinase RNA-like endoplasmic reticulum kinase (PERK)/eukaryotic initiation factor 2 α (eIF2α) by Western blot and an immunofluorescence assay in 24-hour TNF-α-treated 3T3-L1 adipocytes with artificial manipulation of AMPK activation.
Results: Enhancement of AMPK activity by the addition of activator minoimidazole carboxamide ribonucleotide (AICAR) suppressed TNF-α-induced lipolysis, whereas the addition of compound C, an inhibitor of AMPK phosphorylation, enhanced lipolysis. Perilipin, a lipid droplet-associated protein, was decreased by TNF-α and recovered following treatment with AICAR, showing a correlation with the antilipolytic effect of AICAR. Significant activation of PERK/eIF2α, a component of the unfolded protein response signaling pathway, was observed in TNF-α or vesicle-treated 3T3-L1 adipocytes. The antilipolytic effect and recovery of perilipin expression by AICAR in TNF-α-treated 3T3-L1 adipocytes were significantly diminished by treatment with 2-aminopurine, a specific inhibitor of eIF2α.
Conclusion: These data indicated that AICAR-induced AMPK activation attenuates TNF-α-induced lipolysis via preservation of perilipin in 3T3-L1 adipocytes. In addition, PERK/ eIF2α activity is a novel mechanism of the anti-lipolytic effect of AICAR.
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Collections - Medicine > Department of Medicine > 1. Journal Articles
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