The effect of lipid metabolism disorder on patients with hyperuricemia using Multi-Omics analysis

A multiomics study was conducted to investigate how lipid metabolism disorders affect the immune system in Xinjiang patients with hyperuricemia. The serum of 60 healthy individuals and 60 patients with hyperuricemia was collected. This study used LC-MS and HPLC to analyze differential lipid metabolites and enrichment pathways. It measured levels of immune factors tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), carnitine palmitoyltransferase-1 (CPT1), transforming growth factor-beta 1 (TGF-beta 1), glucose (Glu), lactic acid (LD), interleukin 10 (IL-10), and selenoprotein 1 (SEP1) using ELISA, as well as to confirm dysregulation of lipid metabolism in hyperuricemia. 33 differential lipid metabolites were significantly upregulated in patients with hyperuricemia. These lipid metabolites were involved in arachidonic acid metabolism, glycerophospholipid metabolism, linoleic acid metabolism, glycosylphosphatidylinositol (GPI)-anchor biosynthesis, and alpha-Linolenic acid metabolism pathways. Moreover, IL-10, CPT1, IL-6, SEP1, TGF-beta 1, Glu, TNF-alpha, and LD were associated with glycerophospholipid metabolism. In patients with hyperuricemia of Han and Uyghur nationalities, along with healthy individuals, significant differences in CPT1, TGF-beta 1, Glu, and LD were demonstrated by ELISA (P < 0.05). Furthermore, the levels of SEP1, IL-6, TGF-beta 1, Glu, and LD differed considerably between groups of the same ethnicity (P < 0.05). It was found that 33 kinds of lipid metabolites were significantly different in patients with hyperuricemia, which mainly involved 5 metabolic pathways. According to the results of further studies, it is speculated that CPT1, TGF-beta 1, SEP1, IL-6, Glu and LD may increase fatty acid oxidation and mitochondrial oxidative phosphorylation in patients through glycerophospholipid pathway, reduce the rate of glycolysis, and other pathways to change metabolic patterns, promote different cellular functions, and thus affect the disease progression in patients with hyperuricemia.