LPS stimulating upregulates lipid accumulation in mice liver dependent on STAT1/APOE axis signaling pathway.

Lipid metabolism plays a crucial role in maintaining metabolic homeostasis, and its dysregulation is implicated in various disorders. Recent studies have shown that inflammation, particularly that induced by bacterial endotoxins like lipopolysaccharide (LPS), can significantly impact lipid metabolism. However, the mechanisms by which LPS modulates lipid metabolism remain unclear, and the crosstalk between inflammatory signaling and lipid regulatory pathways is not fully understood. To address this gap, this study investigates the effects of LPS on lipid metabolism using animal models. By examining the molecular and physiological responses to LPS exposure, we identify the STAT1/APOE axis as a key pathway through which LPS influences lipid metabolism. Our findings suggest that LPS stimulation enhances lipid metabolism via this axis, providing new insights into the metabolic effects of inflammatory signaling. Notably, our results also highlight an intriguing aspect: short-term LPS exposure may exert beneficial effects on metabolic signaling, challenging the traditional view that inflammation is solely detrimental to metabolism. These findings contribute to a deeper understanding of the relationship between inflammation and lipid metabolism and may have implications for metabolic disease research and therapeutic strategies.