ABCG2 expression and uric acid metabolism of the intestine in hyperuricemia model rat

Morimoto, Chikayuki; Tamura, Yoshifuru; Asakawa, Shinichiro; Kuribayashi-Okuma, Emiko; Nemoto, Yoshikazu; Li, Jinping; Murase, Takayo; Nakamura, Takashi; Hosoyamada, Makoto; Uchida, Shunya; Shibata, Shigeru

doi:10.1080/15257770.2019.1694684

Cited by 16 publications

(11 citation statements)

References 31 publications

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“…The up-regulation of ABCG2 expression in kidney and ileum benefited to the elimination of UA from the body in the HUA rats [12]. In this study, the AST administration significantly increased the mRNA and protein expressions of secretion proteins (OAT1, OAT3 and ABCG2), indicating the facilitated secretion of UA in the high fructose-induced rat models.…”

Section: Effects Of Ast On Mrna and Protein Expressions Of Urate Transporters In Kidneysupporting

confidence: 53%

“…Urate is absorbed by OAT1 and OAT3 from the blood through the basement membrane, which then enters to the renal proximal tubule epithelial cells, and releases through the lumen membrane [11]. Afterwards, the urate is excreted into the lumen of the proximal tubule of nephron with the help of the urate excretion transporter ATP binding cassette superfamily G 2 (ABCG2) [12]. The reabsorption of urate is mainly mediated by glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1).…”

Section: Introductionmentioning

confidence: 99%

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Anti-Hyperuricemic Effects of Astaxanthin by Regulating Xanthine Oxidase, Adenosine Deaminase and Urate Transporters in Rats

Zhou

Zheng

et al. 2020

Marine Drugs

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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.

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Section: Effects Of Ast On Mrna and Protein Expressions Of Urate Transporters In Kidneysupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Anti-Hyperuricemic Effects of Astaxanthin by Regulating Xanthine Oxidase, Adenosine Deaminase and Urate Transporters in Rats

Zhou

Zheng

et al. 2020

Marine Drugs

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“…In addition, Morimoto et al found that the expression of ABCG2 in an HUA rat group was up-regulated in the intestinal villi and crypt. They confirmed that ABCG2 is involved in the intestinal excretion of UA in humans and rats as an extrarenal excretion pathway, thereby providing some clarification regarding UA metabolism along the intestine by focusing on a novel UA exporter, ABCG2 [126]. Furthermore, Wang et al [127] confirmed that chicory extract ameliorates intestinal UA elimination by modulating the ABCG2 transporter.…”

Section: Enhancement In Intestinal Ua Secretionmentioning

confidence: 87%

Bioactive Compounds from Plant-Based Functional Foods: A Promising Choice for the Prevention and Management of Hyperuricemia

Jiang

Gong

et al. 2020

Foods

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Hyperuricemia is a common metabolic disease that is caused by high serum uric acid levels. It is considered to be closely associated with the development of many chronic diseases, such as obesity, hypertension, hyperlipemia, diabetes, and cardiovascular disorders. While pharmaceutical drugs have been shown to exhibit serious side effects, and bioactive compounds from plant-based functional foods have been demonstrated to be active in the treatment of hyperuricemia with only minimal side effects. Indeed, previous reports have revealed the significant impact of bioactive compounds from plant-based functional foods on hyperuricemia. This review focuses on plant-based functional foods that exhibit a hypouricemic function and discusses the different bioactive compounds and their pharmacological effects. More specifically, the bioactive compounds of plant-based functional foods are divided into six categories, namely flavonoids, phenolic acids, alkaloids, saponins, polysaccharides, and others. In addition, the mechanism by which these bioactive compounds exhibit a hypouricemic effect is summarized into three classes, namely the inhibition of uric acid production, improved renal uric acid elimination, and improved intestinal uric acid secretion. Overall, this current and comprehensive review examines the use of bioactive compounds from plant-based functional foods as natural remedies for the management of hyperuricemia.

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“…Interestingly, in this study, the observed overall expression levels of the protein in the intestine are much higher than in the kidney. In rats, ABCG2 expression in the gut was found to further increase in response to increased blood urate concentrations after oxonate treatment [84]. To study the contribution of ABCG2 in intestinal urate excretion (and renal urate excretion which was already discussed above), oxonate-treated ABCG2 knockout mice were used [51,71] and showed a reduction in intestinal urate elimination by roughly 40-50%.…”

Section: Relevance Of Abcg2 In Extrarenal Urate Eliminationmentioning

confidence: 99%

The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update

Eckenstaler

Benndorf

2021

IJMS

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Urate homeostasis in humans is a complex and highly heritable process that involves i.e., metabolic urate biosynthesis, renal urate reabsorption, as well as renal and extrarenal urate excretion. Importantly, disturbances in urate excretion are a common cause of hyperuricemia and gout. The majority of urate is eliminated by glomerular filtration in the kidney followed by an, as yet, not fully elucidated interplay of multiple transporters involved in the reabsorption or excretion of urate in the succeeding segments of the nephron. In this context, genome-wide association studies and subsequent functional analyses have identified the ATP-binding cassette (ABC) transporter ABCG2 as an important urate transporter and have highlighted the role of single nucleotide polymorphisms (SNPs) in the pathogenesis of reduced cellular urate efflux, hyperuricemia, and early-onset gout. Recent publications also suggest that ABCG2 is particularly involved in intestinal urate elimination and thus may represent an interesting new target for pharmacotherapeutic intervention in hyperuricemia and gout. In this review, we specifically address the involvement of ABCG2 in renal and extrarenal urate elimination. In addition, we will shed light on newly identified polymorphisms in ABCG2 associated with early-onset gout.

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ABCG2 expression and uric acid metabolism of the intestine in hyperuricemia model rat

Cited by 16 publications

References 31 publications

Anti-Hyperuricemic Effects of Astaxanthin by Regulating Xanthine Oxidase, Adenosine Deaminase and Urate Transporters in Rats

Anti-Hyperuricemic Effects of Astaxanthin by Regulating Xanthine Oxidase, Adenosine Deaminase and Urate Transporters in Rats

Bioactive Compounds from Plant-Based Functional Foods: A Promising Choice for the Prevention and Management of Hyperuricemia

The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update

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