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9 The pathogenic mechanism underlying ARDS remains largely unclear and there are currently no specific drugs available for its effective treatment in clinical practice

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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 )