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These metabolic pathways interact deeply with core mechanisms such as OS, mitochondrial dysfunction, and abnormal -syn aggregation, collectively forming the complex metabolic background of PD

Wallin R, Hutson S

Excessive FAs in the circulatory system promote insulin secretion from pancreatic beta cells, upregulate the expression of renal uric acid reabsorption proteins Glucose transporter type 9 (GLUT9) and urate transporter 1 (URAT1), and reduce the level of uric acid excretion protein ATP-binding cassette transporter G2 (ABCG2), resulting in elevated serum uric acid levels ( Figure 4 )