Hydrogen peroxide-induced translocation of glycolipid-anchored (c)AMP-hydrolases to lipid droplets mediates inhibition of lipolysis in rat adipocytes.
作者： G Müller , S Wied , C Jung , S Over
DOI: 10.1038/BJP.2008.146
关键词:
摘要: Background: The insulin-independent inhibition of lipolysis by palmitate, the anti-diabetic sulphonylurea glimepiride and H2O2 in rat adipocytes involves stimulation glycosylphosphatidylinositol (GPI)-specific phospholipase-C (GPI-PLC) subsequent translocation GPI-anchored membrane ectoproteins (GPI-proteins), Gce1 cluster differentiation antigen (CD73), from specialized plasma microdomains (DIGs) to cytosolic lipid droplets (LDs). This results cAMP degradation at LD surface failure activate hormone-sensitive lipase. Reactive oxygen species (ROS) may trigger this sequence events response palmitate glimepiride. Experimental approach: The effects various inhibitors ROS production on release H2O2, GPI anchor cleavage photoaffinity-labelled or metabolically labelled CD73 DIGs different fatty acids sulphonylureas were studied with primary adipocytes. Key results: Glimepiride induced via NADPH oxidase mitochondrial complexes I III, respectively. Inhibition was accompanied loss (i) GPI-PLC activation, (ii) (iii) glimepiride. Non-metabolizable drug tolbutamide inactive. activities colocalized stimulated but not tolbutamide. Conclusions implications: The data suggest that mediate activation GPI-protein which leads anti-lipolytic mechanism be engaged future drugs. British Journal Pharmacology (2008) 154, 901–913; doi:10.1038/bjp.2008.146; published online 5 May 2008
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