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TL;DR
This preclinical study used cell lines to show that sodium acetate can both increase and decrease inflammatory macrophage activity in a dose-dependent manner, which then bidirectionally influences lipid accumulation in hepatocytes.
International Journal of Molecular Sciences · 5 authors, 3 centres
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This preclinical study used cell lines to show that sodium acetate can both increase and decrease inflammatory macrophage activity in a dose-dependent manner, which then bidirectionally influences lipid accumulation in hepatocytes.
The study investigated the dose-dependent effects of sodium acetate (NaA) on macrophage activity and subsequent hepatocyte lipid metabolism using RAW264.7 and Kupffer cell lines stimulated with LPS. Researchers treated cells with varying concentrations of NaA. They found that a low dose (0.1 mM) increased pro-inflammatory cytokine expression, phosphorylation of NF-κB p65 and c-Jun, and M1 polarization. In contrast, a high dose (2 mM) reduced these inflammatory responses. The mechanism involved changes in intracellular acetate concentration and activation of the PPARγ/UCP2/AMPK signaling pathway, independent of GPR43 or HDAC inhibition. NaA also regulated lipid accumulation in both macrophages and hepatocytes. The findings suggest a potential bidirectional regulatory role for NaA in NAFLD pathology via macrophage-hepatocyte interactions.