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Updated: Aug 3, 2025

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Intestinal uric acid excretion contributes to serum uric acid decrease during acute gout attack.

Tianyi Zhao1,2, Ling Cao1,2, Cong Lin1,2

  • 1Division of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China.

Rheumatology (Oxford, England)
|April 12, 2023
PubMed
Summary
This summary is machine-generated.

Serum uric acid (SUA) levels decrease during gout attacks due to increased intestinal uric acid excretion. This process involves inflammation-induced activation of the PI3K/Akt pathway and upregulation of ABCG2 transporter expression in intestinal cells.

Keywords:
ABCG2Gouthyperuricemiaintestineuric acid

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Area of Science:

  • Biochemistry
  • Immunology
  • Gastroenterology

Background:

  • Spontaneous decrease in serum uric acid (SUA) during acute gout attacks is a known phenomenon.
  • The underlying mechanisms for this SUA reduction remain largely unclear.

Purpose of the Study:

  • To investigate the spontaneous regulation of SUA during gout attacks.
  • To elucidate the mechanisms behind SUA decrease, focusing on intestinal uric acid excretion and related molecular pathways.

Main Methods:

  • Evaluated SUA levels, serum CRP, and IL-1β in gout patients and a monosodium urate (MSU)-induced gout mouse model.
  • Assessed intestinal uric acid excretion and ATP-binding cassette super-family G member 2 (ABCG2) expression in wild-type and ABCG2-/- mice.
  • Utilized Caco2 cell transwell cultures to study urate transport and analyzed the PI3K/Akt pathway and ABCG2 expression via PCR, western blotting, and immunofluorescence.

Main Results:

  • SUA decreased during acute gout attacks in both human patients and mice, correlating with increased serum CRP and IL-1β.
  • Intestinal uric acid excretion and ABCG2 expression were upregulated in mice during gout attacks.
  • ABCG2 deficiency impaired intestinal uric acid excretion during gout attacks.
  • In vitro studies showed inflammation-induced upregulation of ABCG2 and the PI3K/Akt pathway in intestinal cells, with PI3K/Akt inhibition reducing ABCG2 expression and urate transport.

Conclusions:

  • Increased intestinal urate excretion is responsible for the spontaneous SUA downregulation during acute gout attacks.
  • Inflammation-mediated activation of the PI3K/Akt pathway and subsequent ABCG2 upregulation in intestinal epithelial cells likely drives enhanced intestinal uric acid excretion.