银屑病—肥胖共病的代谢物互作:代谢组学驱动机制的研究进展OA

Research has found that both psoriasis and obesity exhibit disturbances in energy metabolism,such as impaired fatty acid β-oxidation.They share significant elevations in the levels of branched-chain amino acids and aromatic amino acids,constituting characteristic metabolic re-programming of amino acids,accompanied by remodeling of complex lipid homeostasis involving phospholipids,sphingolipids,and steroid metabolism.In-depth analysis indicates that these shared metabolic abnormalities form a"metabolic-inflammatory"vicious cycle by persistently acti-vating key inflammatory pathways such as mTOR and NF-κB and perturbing inflammatory regulato-ry hubs like tryptophan-kynurenine metabolism.This cycle acts as a"metabolic bridge"linking the two diseases.Animal studies further suggest that saturated fatty acid/bile acid metabolism disorders and neutrophil extracellular traps(NETs)are key links in the aggravation of psoriasis by obesity.These findings provide new integrated perspectives for understanding the comorbidity mechanisms of psoriasis and obesity,and also offer a theoretical basis for future discovery of co-morbidity biomarkers and development of intervention strategies targeting shared metabolic path-ways.This article aims to systematically review the potential metabolic basis of the comorbidity be-tween psoriasis and obesity by integrating metabolomics data.