Channel Function of TRPML1 Prompts Lipolysis in Mature Adipocytes
10.11620/IJOB.2018.43.1.023
- Author:
Mi Seong KIM
1
;
Min Seuk KIM
Author Information
1. Center for Metabolic Function Regulation, School of Medicine, No. 460, Wonkwang University, Iksan-Daero, Iksan, Jeonbuk 54538, Republic of Korea.
- Publication Type:Original Article
- Keywords:
Transient receptor potential mucolipin1;
lipolysis;
ML-SA1;
adipocyte
- MeSH:
Adipocytes;
Glycerol;
Homeostasis;
Isoproterenol;
Lipid Metabolism;
Lipolysis;
Membranes;
Obesity
- From:International Journal of Oral Biology
2018;43(1):23-27
- CountryRepublic of Korea
- Language:English
-
Abstract:
Increased intracellular levels of Ca²⁺ are generally thought to negatively regulate lipolysis in mature adipocytes, whereas store-operated Ca²⁺ entry was recently reported to facilitate lipolysis and attenuate lipotoxicity by inducing lipophagy. Transient receptor potential mucolipin1 (TRPML1), a Ca²⁺-permeable non-selective cation channel, is mainly expressed on the lysosomal membrane and plays key roles in lysosomal homeostasis and membrane trafficking. However, the roles of TRPML1 in lipolysis remains unclear. In this study, we examined whether the channel function of TRPML1 induces lipolysis in mature adipocytes. We found that treatment of mature adipocytes with ML-SA1, a specific agonist of TRPML1, solely upregulated extracellular glycerol release, but not to the same extent as isoproterenol. In addition, knockdown of TRPML1 in mature adipocytes significantly reduced autophagic flux, regardless of ML-SA1 treatment. Our findings demonstrate that the channel function of TRPML1 partially contributes to lipid metabolism and autophagic membrane trafficking, suggesting that TRPML1, particularly the channel function of TRPML1, is as therapeutic target molecule for treating obesity.
