Abstract

Hyperuricemia is a central risk factor for gout and increases the risk for other chronic diseases, including cardiometabolic disease, kidney disease, and hypertension. Overproduction of urate is one of the main reasons for hyperuricemia, and dietary factors including seafoods, meats, and drinking are contributed to the development of it. However, the lack of a suitable animal model for urate metabolism is one of the main reasons for the delay and limitations of hyperuricemia research. Combining evolutionary biological studies and clinical studies, we conclude that chicken is a preferred animal model for hyperuricemia. Thus, we provided chickens a high-protein diet (HPD) to evaluate the changes in the serum urate levels in chickens. In our study, the HPD increased the serum urate level and maintained it at a long-term high level in chickens. Long-term high serum urate levels induced an abnormal chicken claw morphology and the precipitation of monosodium urate (MSU) in joint synovial fluid. In addition, a long-term HPD also decreased the glomerular filtration rate and induced mild renal injury. Most importantly, allopurinol and probenecid displayed the positive effects in decreasing serum urate and then attenuated hyperuricemia in chicken model. These findings provide a novel model for hyperuricemia and a new opportunity to further investigate the effects of long-term hyperuricemia on other metabolic diseases.

Highlights

  • Hyperuricemia is a metabolic disease caused by a purine metabolism disorder and is characterized by a serum urate level greater than 420 μmol/L or 360 μmol/L [1]

  • High-density lipoprotein cholesterol (HDL-C), apolipoprotein A-I (ApoA1), apolipoprotein B (ApoB), glucose (GLU), lactate dehydrogenase (LDH), total protein (TP), albumin (ALB), alkaline phosphatase (ALP), P, Ca, K, Na, and Cl were shown to have no difference between the control diet (CON) and high-protein diet (HPD) group

  • We demonstrated that HPD can increase the serum urate level in white leghorns chickens within 2 weeks, which gradually declined within 6 weeks and was maintained at a relatively high level until the end of the experiment

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Summary

Introduction

Hyperuricemia is a metabolic disease caused by a purine metabolism disorder and is characterized by a serum urate level greater than 420 μmol/L (male) or 360 μmol/L (female) [1]. In an evolutionary biology study, it was found that the uricase in humans and gorillas was mutated 16-24 million years ago; the final product of purine metabolism is urate (Figure 1) [20]. Other mammals, such as rats, mice, and rabbits, contain uricase and can metabolize urate to allantoin, which is soluble in water and easy to excrete [21]. Chickens could be a suitable animal model for urate metabolism and gout studies. In the purine-urate metabolic pathway, chickens are more suitable for studying hyperuricemia and gout disease than rodents, such as mice. Several studies have demonstrated that birds have another pathway to metabolize urate, mainly due to antioxidation ability of urate [24]

HPD Increases Serum Levels of Urate in Chickens
HPD Induces an Abnormal Claw Morphology in Chickens
HPD Induces MSU Crystal Production in Synovial Fluid and Other Tissue Fluids
HPD Induces Renal Injury in Chickens
Phylogenetic Tree Construction
Animals and Experimental Design
Histological Analysis
Radiographic Imaging
Biochemical Analysis
Gene Expression Analysis
Statistical Analysis
Findings
Conclusions
Full Text
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