ArticlePloS one2022
Uricase-deficient rats with similarly stable serum uric acid to human's are sensitive model animals for studying hyperuricemia.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 17 citations in OpenAlex.
- Polydatin alleviates adenine-induced nephropathy in mice.Renal failure · 2026Article
- ABCG2 transporter: Structural and functional associations with gout (Review).International journal of molecular medicine · 2026Review
- A review of the evidence for a protective role of uric acid in Parkinson's disease.NPJ Parkinson's disease · 2025Review
- Designer probiotic-based living drugs for uric acid homeostasis control in hyperuricemic mice and rats.Cell reports. Medicine · 2025Article
- Sex differences in ventricular muscle energetics in a type 2 diabetic rat model.Cardiovascular diabetology. Endocrinology reports · 2025Article
- A simple and rapid colorimetric sensor for uric acid detection based on ligand-modified silver nanoparticles with oxidase activity.Mikrochimica acta · 2025Article
- Uricase deficiency in rats results in a variety of metabolic disorders, addition to gouty nephropathy.PloS one · 2025Article
- Progress in animal models for studying hyperuricemia.Frontiers in pharmacology · 2025Review
- Progress in modeling avian hyperuricemia and gout (Review).Biomedical reports · 2025Review
- Uric acid reduces the expression of aquaporins in renal collecting ducts to increase urine output in hyperuricemia.Frontiers in physiology · 2025Article
- Raising serum uric acid with a uricase inhibitor worsens PKD in rat and mouse models.American journal of physiology. Renal physiology · 2024Article
- Genes Selectively Expressed in Rat Organs.Current genomics · 2024Article
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7 authors at 2 institutions in 1 country.
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Abstract
The aim of this study was to provide a sensitive model animal for studying hyperuricemia. Male uricase-deficient rats, named Kunming-DY rats, were raised for 130 days, or orally administered with purines and other chemicals. Serum uric acid (SUA) in the animals was assayed, and the UA level in their organs and their 24-h excretion was determined. Genes in the jejunum, ileum, kidney and liver related to UA synthesis and transportation were detected by quantitative RNA sequencing. Uricase-deficient rats have a high level of SUA and are sensitive to xanthine, adenosine, inosine, allopurinol, and alcohol. Besides, the high level of SUA in male uricase-deficient rats was stable, much higher than that in wild-type rats but similar to that in men. The distribution pattern of UA in uricase-deficient rats' organs was different from that in wild-type rats. The kidney, liver, and small intestine were the top three organs where UA distributed, but the UA in the small intestine, colon, lung, thymus, and brain was less affected by uricase deficiency, indicating that these organs are constitutive distribution organs in UA. The 24-h UA excreted by a uricase-deficient rat was about five times higher than that excreted by a wild-type rat. However, the 24-h UA excreted through feces was not significantly changed. Both the urine volume and UA in uricase-deficient rats significantly increased, and more than 90% of UA was excreted via urine. The expression of xanthine dehydrogenase was not upregulated. Some genes of transporter associated with uric acid excretion in the kidney were significantly regulated, though not sufficient to explain the increase in SUA. In conclusion, male uricase-deficient rats' UA metabolism is similar to that of men. The elevation of SUA in uricase-deficient rats is caused by uricase deficiency, and uricase-deficient rats are a sensitive model for studying hyperuricemia.
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