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Dehydroepiandrosterone activates 5'-adenosine monophosphate-activated protein kinase and suppresses lipid accumulation and adipocyte differentiation in 3T3-L1 cells.
Metadata
Journalbiochemical and biophysical research communications2.985Date
2020 Jun 03
4 months ago
Type
Journal Article
Volume
2020-Jul-30 / 528 : 612-619
Author
Yokokawa T 1, Sato K 2, Narusawa R 3, Kido K 4, Mori R 3, Iwanaka N 5, Hayashi T 6, Hashimoto T 3
Affiliation
  • 2. Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.
  • 3. Faculty of Sport and Health Science, Ritsumeikan University, Shiga, Japan.
  • 4. Faculty of Sport and Health Science, Ritsumeikan University, Shiga, Japan; Faculty of Sports and Health Science, Fukuoka University, Fukuoka, Japan.
  • 5. Faculty of Sport and Health Science, Ritsumeikan University, Shiga, Japan; Faculty of Health Science, Kyoto Koka Women's University, Kyoto, Japan.
  • 6. Laboratory of Sports and Exercise Medicine, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto, Japan.
Doi
PMIDMESH
Abstract
Substantial evidence has linked dehydroepiandrosterone (DHEA) levels to the anti-obesity and anti-diabetic effects of exercise. While 5'-adenosine monophosphate-activated protein kinase (AMPK) is a negative regulator of adipocyte differentiation and lipid accumulation, activation of mammalian target of rapamycin complex 1 (mTORC1), which is inhibited by AMPK, is required for adipocyte differentiation and positively regulates lipid accumulation. DHEA treatment activates the AMPK pathway in C2C12 myotubes. Hence, DHEA addition to preadipocytes and adipocytes might activate AMPK and inhibit mTORC1, resulting in the inhibition of adipogenesis and lipid accumulation. Therefore, we investigated the effect of DHEA on the AMPK pathway, mTORC1 activity, adipocyte differentiation, and lipid accumulation in 3T3-L1 cells. DHEA suppressed lipid accumulation and adipogenic marker expression during differentiation. It also activated AMPK signaling in preadipocytes and adipocytes and suppressed mTORC1 activity during differentiation. These results suggest that the activation of the AMPK pathway and inhibition of mTORC1 activity may mediate the anti-obesity effect of DHEA, providing novel molecular-level insights into its physiological functions.
Keywords: AMPK Adipocyte Adipogenesis Dehydroepiandrosterone mTORC1
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Biochem Biophys Res Communbiochemical and biophysical research communications
Metadata
LocationUnited States
FromACADEMIC PRESS INC ELSEVIER SCIENCE

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