Conjugated Linoleic Acid Ameliorates High Fructose‐Induced Hyperuricemia and Renal Inflammation in Rats via NLRP3 Inflammasome and TLR4 Signaling Pathway

Scope Conjugated linoleic acid (CLA), a bioactive substance predominantly found in ruminant products, improves insulin resistance and exhibits anti‐inflammatory activity. The chief objective of the study is to investigate the effects and potential mechanisms of CLA on high fructose‐induced hyperuricemia and renal inflammation. Methods and results Hyperuricemia and renal inflammation are induced in rats by 10% fructose. Hyperuricemia, insulin resistance, and renal inflammation are evaluated. CLA potently ameliorates fructose‐induced hyperuricemia with insulin resistance and significantly reduces the levels of inflammation factors in serum and kidney. It reverses fructose‐induced upregulation of glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1) in the kidney. Moreover, CLA dramatically inhibits the activation of the nucleotide‐binding oligomerization domain–like receptor family pyrin domain‐containing 3 (NLRP3) inflammasome. Additionally, CLA suppresses toll‐like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling activation to inhibit nuclear factor‐kB (NF‐kB) signaling in the kidney of fructose‐fed rats. Conclusion CLA ameliorates hyperuricemia along with insulin resistance and renal inflammatory, which may be associated with the suppression of renal GLUT9 and URAT1 in fructose‐fed rats. Its molecular mechanism may be related to the inhibition of NLRP3 inflammasome and TLR4/MyD88 signaling pathway. Therefore, CLA may be a promising candidate for preventing fructose‐induced hyperuricemia and renal inflammation.