Abstract

Uricase-deficient rats could be one of the optimal model animals to study hyperuricemia. The present study aimed to find the biological differences between uricase-deficient (Kunming-DY rats) and wild-type male rats. Uricase-deficient rats and wild-type rats were commonly bred. Their body weight, water and food consumption, 24-h urine and feces, uric acid in serum and organs, and serum indexes were recorded or assayed. Organs, including the heart, liver, spleen, lung, kidney, thymus, stomach, duodenum, and ileum, were examined using a routine hematoxylin-eosin staining assay. We found that the growth of male uricase-deficient rats was retarded. These rats excreted more urine than the wild-type rats. Their organ indexes (organ weight body weight ratio), of the heart, liver, kidney, and thymus significantly increased, while those of the stomach and small intestine significantly decreased. The uricase-deficient rats had a significantly higher level of serum uric acid and excreted more uric acid via urine at a higher concentration. Except for the liver, uric acid increased in organs and intestinal juice of uricase-deficient rats. Histological examination of the uricase-deficient rats showed mild injuries to the heart, liver, spleen, lung, kidney, thymus, stomach, duodenum, and ileum. Our results suggest that uricase-deficient rats have a different biological pattern from the wild-type rats. Uricase deficiency causes growth retardation of young male rats and the subsequent increase in serum uric acid results in mild organs injuries, especially in the kidney and liver.

Highlights

  • Hyperuricemia is regarded as a vital factor for the development of gout, renal dysfunction, and osteoarthritis [1]

  • The present study systematically investigated the biological properties of the urate oxidase (Uox)-/rats to clarify whether these rats may be an alternative model animal to study hyperuricemia and associated diseases

  • The results suggest that uricase deficiency retards the growth of rats

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Summary

Introduction

Hyperuricemia is regarded as a vital factor for the development of gout, renal dysfunction, and osteoarthritis [1]. It is regarded as a risk factor closely correlated with hypertension, type 2 diabetes mellitus, and hyperlipidemia [2, 3]. Previous reports have suggested that hyperuricemia is tangled with the injuries to the intestinal tract [4], liver [5] and heart failure [6]. Hyperuricemia and associated disorders cause a significant economic burden on modern society.

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