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Rather than functioning merely as passive lipid storage depots, LDs serve as active innate immune hubs that concentrate lipid metabolic enzymes (such as cyclooxygenases and lipoxygenases) to drive the robust synthesis of potent pro-inflammatory lipid mediators, including eicosanoids and prostaglandins, which intertwined with classic lipid-mediated inflammatory signaling pathways (102)
Conversion to NADH sustains mitochondrial electron transport, whereas NADPH supports reductive biosynthesis and glutathione-dependent antioxidant buffering [83]
CMAJ 2009
When adding GLP-1-R-Antagonist Exendin (9-36), the effects of Liraglutide were reversed, indicating receptor-mediated action [13]
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