Stomatin modulates adipogenesis through ERK pathway and regulates fatty acid uptake and lipid droplet growth
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ABSTRACT: Controlling 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 rafts, 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, as well as 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 diets exhibit obesity, insulin resistance and hepatic impairments; however, such phenotypes are not seen if feeding the transgenic animals with regular diets. Inhibitions of stomatin by gene knockdown or OB-1 pharmacological treatments inhibit adipogenic differentiation and LD growth through downregulation of PPARγ pathway. Effects of stomatin on PPARγ involve ERK signaling; however, an alternate pathway may also exist.
INSTRUMENT(S): LTQ Orbitrap Velos
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Cell Culture
SUBMITTER: Chen-Chung Liao
LAB HEAD: Chen-Chung Liao
PROVIDER: PXD031866 | Pride | 2022-07-05
REPOSITORIES: Pride
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