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Magnolol promotes thermogenesis and attenuates oxidative stress in 3T3-L1 adipocytes.
- Source :
-
Nutrition (Burbank, Los Angeles County, Calif.) [Nutrition] 2018 Jun; Vol. 50, pp. 82-90. Date of Electronic Publication: 2018 Feb 05. - Publication Year :
- 2018
-
Abstract
- Objective: The aim of this study was to explore the browning and antioxidative effects of magnolol in 3T3-L1 adipocytes, as recruitment of beige-like adipocytes (browning) by natural compounds is being considered as a promising strategy to fight against obesity.<br />Methods: Magnolol-induced browning effect was evaluated by determining the expression levels of specific marker genes and proteins using real-time polymerase chain reaction and immunoblotting, respectively. Induction of thermogenesis and suppression of oxidative stress in 3T3-L1 adipocytes were further validated by immunofluorescence.<br />Results: Magnolol significantly enhanced expression of a core set of brown fat-specific marker genes (Ucp1, Cd137, Prdm16, Cidea, and Tbx1) and proteins (UCP1, PRDM16, and PGC-1α). Increased expression of UCP1 and other brown fat-specific markers contributed to the browning of 3T3-L1 adipocytes possibly via activation of the AMPK, PPARγ, and protein kinase A (PKA) pathways. In addition, magnolol up-regulated key fatty acid oxidation and lipolytic markers (CPT1, ACSL1, SIRT1, and PLIN) and down-regulated lipogenic markers (FAS and SREBP1). Magnolol also reduced the production and release of reactive oxygen species.<br />Conclusion: The current data suggest possible roles for magnolol in browning of white adipocytes, augmentation of lipolysis, and thermogenesis, as well as repression of oxidative stress and lipogenesis. Thus, magnolol may be explored as a potentially promising therapeutic agent for the prevention of obesity and other metabolic disorders.<br /> (Copyright © 2018 Elsevier Inc. All rights reserved.)
- Subjects :
- 3T3-L1 Cells cytology
Adipose Tissue, Brown metabolism
Animals
Apoptosis Regulatory Proteins metabolism
Cell Culture Techniques
DNA-Binding Proteins metabolism
Lipogenesis drug effects
Lipolysis drug effects
Mice
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha metabolism
T-Box Domain Proteins metabolism
Transcription Factors metabolism
Tumor Necrosis Factor Receptor Superfamily, Member 9 metabolism
Uncoupling Protein 1 metabolism
Adipocytes metabolism
Antioxidants pharmacology
Biphenyl Compounds pharmacology
Lignans pharmacology
Oxidative Stress drug effects
Thermogenesis drug effects
Subjects
Details
- Language :
- English
- ISSN :
- 1873-1244
- Volume :
- 50
- Database :
- MEDLINE
- Journal :
- Nutrition (Burbank, Los Angeles County, Calif.)
- Publication Type :
- Academic Journal
- Accession number :
- 29547798
- Full Text :
- https://doi.org/10.1016/j.nut.2018.01.017