The effect of lipid metabolism disorder on the immune microenvironment in Xinjiang patients with hyperuricemia using Multi-Omics analysis

Abstract Objectives The characteristics of lipid metabolism and key pathway regulatory factors in Xinjiang hyperuricemia patients were analyzed by multiomics to observe the influence of lipid metabolism disorder on the immune microenvironment in Xinjiang patients with hyperuricemia. Methods Serum samples were collected from 60 hyperuricemia patients (case group) and 60 normal people (control group). We analyzed the differential lipid metabolites and enrichment pathways in two groups by using high-performance liquid chromatography (HPLC) and liquid chromatography-mass spectrometry (LC-MS). We measured the levels of immune factors CPT1, SEP1, IL-6, IL-10, TNF-α, TGF-β1, Glu, and LD by an enzyme-linked immunosorbent assay (ELISA) and verified dysregulation of lipid metabolism in hyperuricemia. Results The results demonstrated that the 33 differential lipid metabolites were significantly upregulated in hyperuricemia patients. These lipid metabolites are involved in five metabolic pathways, including glycerophospholipid metabolism, linoleic acid metabolism, alpha-Linolenic acid metabolism, glycosylphosphatidylinositol (GPI)-anchor biosynthesis, and Arachidonic acid metabolism. Moreover, CPT1, SEP1, IL-6, IL-10, TNF-α, TGF-β1, Glu, and LD were associated with the glycerophospholipid metabolism. These regulators may impact hyperuricemia progression by altering metabolic patterns and facilitating different cellular functions. In hyperuricemia patients of Han and Uyghur nationalities, along with healthy individuals, significant differences in CPT1, TGF-1, Glu, and LD were demonstrated by ELISA (p < 0.05). Furthermore, the content of SEP1, IL-6, TGF-β1, Glu, and LD differed considerably between groups of the same ethnicity (p < 0.05). Conclusion Thirty-three differential lipid metabolites involved primarily in the glycerophospholipid metabolic pathway were significantly elevated in hyperuricemia patients compared to healthy individuals. We hypothesized that CPT1、TGF-β1、SEP1、IL-6、Glu, 、LD might influence metabolism and the immune microenvironment in hyperuricemia patients. CPT1, TGF-β1, SEP1, IL-6, Glu, and LD were speculated to increase fatty acid oxidation and mitochondrial oxidative phosphorylation while decreasing glycolysis, affecting metabolism and the immune system microenvironment in hyperuricemia patients.