Elevated uric acid levels are associated with lipid metabolism disorders. The effects of Imperata cylindrica polysaccharide (ICPC-a) were explored using a hyperuricemia mouse model and a uric acid-induced HepG2 hepatocyte model. ICPC-a significantly improved total cholesterol, triglycerides, low-density lipoprotein levels, and hepatic lipid deposition in hyperuricemia mice. The liver/body weight ratio decreased, and markers of liver damage, inflammation, and dyslipidemia improved. Metabolomics analysis suggested that ICPC-a modulates lipid metabolism by influencing the glycerophospholipid pathway and the enzyme LPCAT3. Stable HepG2 cell lines with knocked-down LPCAT3 were constructed, and western blot and RT-PCR were used to assess the impact of its knockdown on lipid metabolism under uric acid stimulation. In cells with reduced LPCAT3 expression, ICPC-a was still able to alleviate uric acid-induced lipid accumulation, though the effect was less pronounced compared to cells with normal LPCAT3 levels. However, the effectiveness was diminished compared to cells where LPCAT3 was not knocked down. These findings indicated that LPCAT3 was an important target through which ICPC-a regulated lipid metabolism disorders induced by hyperuricemia. These discoveries emphasized that ICPC-a, as a prebiotic, could modulate hepatic lipid accumulation and inflammation, contributing to the maintenance of hepatic lipid homeostasis.