Trans-anethole Induces Thermogenesis via Activating SERCA/SLN Axis in C2C12 Muscle Cells

• Published in: Biotechnology and bioprocess engineering Vol. 27; no. 6; pp. 938 - 948
• Main Authors: Mukherjee, Sulagna, Choi, Minji, Yun, Jong Won
• Format: Journal Article
• Language: English
• Published: Seoul The Korean Society for Biotechnology and Bioengineering 01.12.2022; Springer Nature B.V
• Subjects: Adipocytes; Adipose tissue; aerobiosis; Anethole; Biotechnology; Ca2+-transporting ATPase; Chemical compounds; Chemistry; Chemistry and Materials Science; Energy expenditure; Essential oils; fennel; heat production; Industrial and Production Engineering; Lipid metabolism; Lipids; Lipolysis; Metabolism; Molecular docking; muscle development; Muscles; Myoblasts; Myogenesis; Non-shivering; obesity; Oxidative metabolism; Pharmacology; Research Paper; Ryanodine receptors; Shivering; therapeutics; Thermogenesis; anethole; thermogenesis; obesity; UCP1-independent thermoigenesis; C2C12 muscle cells
• ISSN: 1226-8372; 1976-3816
• DOI: 10.1007/s12257-022-0242-2

Recently, adaptive non-shivering thermogenesis has attracted considerable attention because it can elevate energy expenditure and help treat obesity. Despite the numerous reports related to UCP1-driven thermogenesis, little is known regarding UCP1-independent thermogenesis in adipose tissues and muscle. Therefore, it is essential to identify the molecular targets for UCP1-independent thermogenesis and their mechanisms to increase the energy expenditure pharmacologically in both adipocytes and muscle. This study examined whether trans -anethole (TA), a major component of the essential oils of fennel, induces UCP1-independent SERCA/SLN-based thermogenesis and promotes the lipid metabolism in muscle cells. TA enhanced myogenesis, lipolysis, and the oxidative metabolism in C2C12 muscle cells. More importantly, TA activated the SERCA/SLN/RYR axis, thereby inducing thermogenesis in muscle cells. Molecular docking analysis revealed a good interaction between SERCA with TA with a strong bind activity. In conclusion, the current data unveiled a previously unknown mechanism of TA in myoblasts and suggests a possible therapeutic agent in muscles by enhancing energy expenditure.