Abstract
Sestrin2, a well-known adenosine monophosphate-activated protein kinase (AMPK) regulator, plays a protective role against metabolic stress. The β3-adrenergic receptor (β3AR) induces fat browning and inhibits muscle atrophy in an AMPK-dependent manner. However, no prior research has examined the relationship of sestrin2 with β3AR in body composition changes. In this study, CL 316,243 (CL), a β3AR agonist, was administered to wild-type and sestrin2-knockout (KO) mice for 2 weeks, and fat and muscle tissues were harvested. CL induced AMPK phosphorylation, expression of brown-fat markers, and mitochondrial biogenesis, which resulted in the reduction of lipid droplet size in inguinal white adipose tissue (iWAT). These effects were not observed in sestrin2-KO mice. In CL-treated soleus muscle, sestrin2-KO was related to decreased myogenic gene expression and increased levels of muscle atrophy-related molecules. Our results suggest that sestrin2 is associated with beneficial β3AR-mediated changes in body composition, especially in iWAT and in the soleus.
Original language | English |
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Pages (from-to) | 552-557 |
Number of pages | 6 |
Journal | Endocrinology and Metabolism |
Volume | 12 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2022 Jun |
Bibliographical note
Funding Information:This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF), South Korea, funded by the Ministry of Education (NRF-2020R1I1A1A01072592 and NRF-2021R1A2C2008792) and by a Korea Medical Device Development Fund grant funded by the Korean government (the Ministry of Science and ICT, the Ministry of Trade, Industry and Energy, the Ministry of Health & Welfare, the Ministry of Food and Drug Safety) (Project Number: 9991007469, KMDF_PR_20200901_0233).
Publisher Copyright:
© 2022 Korean Endocrine Society.
Keywords
- Adipose tissue
- Adrenergic beta-3 receptor agonists
- Brown
- Mouse
- Muscle development
- Muscular atrophy
- Sestrin2 protein
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrinology