Fructose and Potassium Oxonate-Induced Hyperuricemia Model

Creative Bioarray is renowned for its expertise in establishing innovative animal models that accurately replicate human diseases. Our commitment to excellence is evident in our meticulously developed hyperuricemia model, which is induced through a combination of fructose and potassium oxonate. This model has been carefully designed to not only simulate the pathophysiological conditions of hyperuricemia but also to be adaptable to your specific research needs. Whether you are exploring the intricacies of disease mechanisms, evaluating novel therapeutic interventions, or validating diagnostic tools, our hyperuricemia model offers a robust platform to advance your research endeavors.

The fructose and potassium oxonate-induced hyperuricemia model offers a compelling approach to studying the mechanisms and treatments of hyperuricemia, leveraging the distinct metabolic pathways influenced by fructose and potassium oxonate. Fructose, predominantly metabolized in the liver by ketohexokinase (fructokinase C, KHK-C, or KHK), leads to the rapid generation of fructose-1-phosphate. This swift reaction depletes ATP and lowers phosphorylation levels, prompting an increase in AMP deaminase activity under conditions of reduced intracellular phosphate. Consequently, AMP is converted to IMP, intensifying the production of uric acid.

In tandem, potassium oxonate, a triazabenzene compound, inhibits uricase activity, further elevating uric acid levels. This dual mechanism--fructose metabolism and uricase inhibition--creates a robust model for hyperuricemia that closely mimics the human condition.

Our Fructose and Potassium Oxonate-Induced Hyperuricemia Model

  • Available Animal

Rat

  • Modeling Method

Animals are administered a daily regimen of fructose dissolved in drinking water, supplemented with intragastric potassium oxonate, over a period of 10 weeks to induce hyperuricemia.

Method for fructose and potassium oxonate-induced hyperuricemia.Fig. 1 Modeling method of fructose and potassium oxonate-induced hyperuricemia model.

  • Endpoints
  • Serum biomarkers: uric acid (UA), creatinine, BUN, etc
  • Kidney observation
  • Histology analysis of kidney: H&E staining, Masson staining
  • qPCR or Western blot
  • Body weight
  • Other customized endpoints: available upon request

Quotation and Ordering

Creative Bioarray is willing to share our state-of-the-art platforms and sufficient expertise with our clients to boost their drug development. If you are interested in our services, please do not hesitate to contact us at any time or submit an inquiry to us directly.

Reference

  1. Xu, Z., et al. Comparison of 3 hyperuricemia mouse models and evaluation of food-derived anti-hyperuricemia compound with spontaneous hyperuricemia mouse model. Biochemical and Biophysical Research Communications, 2022, 630: 41-49.

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For research use only. Not for any other purpose.