Abstract
This study was designed to investigate the effects and underlying mechanisms of Astaxanthin (AST) on high-fructose-induced hyperuricemia (HUA) from the perspectives of the uric acid (UA) synthesis and excretion in rat models. Following six weeks of a 10% fructose diet, the level of serum UA effectively decreased in the AST groups as compared to the model group. The enzymatic activities of xanthine oxidase (XOD) and adenosine deaminase (ADA) were significantly inhibited, and the mRNA expression levels of XOD and ADA significantly decreased after the AST administration. These results suggested that the AST reduced UA synthesis by inhibiting the mRNA expressions and enzyme activities of XOD and ADA, thereby contributing to HUA improvement. On the hand, the relative expressions of the mRNA and protein of kidney reabsorption transport proteins (GLUT9 and URAT1) were significantly down-regulated by AST, while that of the kidney secretion proteins (OAT1, OAT3 and ABCG2) were significantly up-regulated by AST. These results indicated that the AST promoted UA excretion by regulating the urate transport proteins, and thus alleviated HUA. This study suggested that the AST could serve as an effective alternative to traditional medicinal drugs for the prevention of fructose-induced HUA.
Highlights
Fructose, a naturally occurring monosaccharide present in fruit, honey, and some vegetables, has plenty of use in processed foods [1]
Thegroup other (Model), allopurinol group (ALL), astaxanthin low-dose group (AST-L), astaxanthin middle-dose groups were divided into five groups, which included; model group (Model), allopurinol group group (AST-M)
The present study investigated the preventive effects of AST on high-fructose-induced hyperuricemia (HUA) in rats
Summary
A naturally occurring monosaccharide present in fruit, honey, and some vegetables, has plenty of use in processed foods [1]. HUA has become a prevalent disease with increasing incidence. The prevalence of gout in American adults has reached to 3.9%, whereas the proportion of young people among the HUA patients is still increasing [3]. HUA is caused by the imbalance of the synthesis and excretion of UA, characterized by high UA levels (serum UA level > 420 μmol/L) [4]. The synthesis of UA primarily occurs in liver. The rapid phosphorylation of fructose requires numerous ATP, which causes reduction in the intracellular
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