Stomatin modulates adipogenesis through the ERK pathway and regulates fatty acid uptake and lipid droplet growth

Shao-Chin Wu, Yuan-Ming Lo, Jui-Hao Lee, Chin-Yau Chen, Tung-Wei Chen, Hong-Wen Liu, Wei-Nan Lian, Kate Hua, Chen-Chung Liao, Wei-Ju Lin, Chih-Yung Yang, Chien-Yi Tung () and Chi-Hung Lin ()
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Shao-Chin Wu: National Yang Ming Chiao Tung University
Yuan-Ming Lo: National Yang Ming Chiao Tung University
Jui-Hao Lee: National Yang Ming Chiao Tung University and Academia Sinica
Chin-Yau Chen: National Yang Ming Chiao Tung University Hospital
Tung-Wei Chen: National Yang Ming Chiao Tung University
Hong-Wen Liu: National Yang Ming Chiao Tung University
Wei-Nan Lian: National Yang Ming Chiao Tung University
Kate Hua: Cancer Progression Research Center, National Yang Ming Chiao Tung University
Chen-Chung Liao: Cancer Progression Research Center, National Yang Ming Chiao Tung University
Wei-Ju Lin: Cancer Progression Research Center, National Yang Ming Chiao Tung University
Chih-Yung Yang: Taipei City Hospital
Chien-Yi Tung: Cancer Progression Research Center, National Yang Ming Chiao Tung University
Chi-Hung Lin: National Yang Ming Chiao Tung University

Nature Communications, 2022, vol. 13, issue 1, 1-17

Abstract: Abstract Regulation of fatty acid uptake, lipid production and storage, and metabolism of lipid droplets (LDs), is closely related to lipid homeostasis, adipocyte hypertrophy and obesity. We report here that stomatin, a major constituent of lipid raft, participates in adipogenesis and adipocyte maturation by modulating related signaling pathways. In adipocyte-like cells, increased stomatin promotes LD growth or enlargements by facilitating LD-LD fusion. It also promotes fatty acid uptake from extracellular environment by recruiting effector molecules, such as FAT/CD36 translocase, to lipid rafts to promote internalization of fatty acids. Stomatin transgenic mice fed with high-fat diet exhibit obesity, insulin resistance and hepatic impairments; however, such phenotypes are not seen in transgenic animals fed with regular diet. Inhibitions of stomatin by gene knockdown or OB-1 inhibit adipogenic differentiation and LD growth through downregulation of PPARγ pathway. Effects of stomatin on PPARγ involves ERK signaling; however, an alternate pathway may also exist.

Date: 2022
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DOI: 10.1038/s41467-022-31825-z

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