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Dear Zefr,

Why did you delete my image. I work in a hospital laboratory and the image at the top of the page shows uric acid needles in synovial fluid in someone with gout. The image I posted of uric acid crystals in urine have a completely different shape and are the cause of kidney stones. Bert Grijsen Laboratorium en Hobby (talk) 08:47, 28 January 2024 (UTC)[reply]

Per the discussion with User:Zefr on my talk page, I am proposing a simplified addition to the Biochemistry section to document the specific enzymatic pathway by which fructose metabolism generates uric acid.

This mechanism is well-established in the literature but currently missing from the article. The goal is to describe the chemical inputs/outputs (stoichiometry) without WP:JARGON or making clinical health claims.

Why this is needed: Current sources (like PubChem) identify uric acid as a product of purine metabolism but do not describe the specific fructose-triggered generation described in recent reviews. The research describes an enzymatic reaction without feedback inhibition, which establishes why high dietary fructose load becomes problematic (unregulated kinetics). Critically, this 'unregulated' mechanism clarifies that the effect is dose-dependent (driven by flux) rather than intrinsic toxicity, aligning the biochemistry with mainstream dietary consensus. This addition fills that gap by explaining the mechanism (ATP consumption) rather than just the outcome.

Proposed Text: "Fructose metabolism produces uric acid via the enzyme ketohexokinase. Unlike glucose metabolism, this pathway is unregulated, meaning it occurs rapidly when intake is high. This rapid processing transiently consumes cellular energy (ATP), leading to the degradation of AMP into uric acid." ^[1][2]

Note on Sourcing: The proposed text relies on recent reviews (Softic 2020, Faienza 2024) to verify the specific kinetics of the enzyme (lack of feedback inhibition). While general databases like PubChem (CID 1175) correctly identify uric acid as a metabolite, they do not detail the upstream fructose-specific driver (KHK-mediated ATP depletion) required to explain this mechanism accurately.

I have removed technical terms like "unrestrained phosphorylation" to meet WP:MTAA standards while preserving the biochemical logic. Potentialmotion (talk) 22:47, 2 January 2026 (UTC)[reply]

Two simple concepts about fructose can be stated in the biochemistry section: 1) low typical amounts of fructose consumed in an ordinary diet have a negligible effect on uric acid levels, and 2) excessive fructose consumption triggers a pathway to higher uric acid production. The Softic and Faienza sources mentioned above focus on the second concept, and so may mislead common readers into believing that any level of fructose consumed will cause hyperuricemia.

A proposed revision with other sources follows: Zefr (talk) 20:17, 3 January 2026 (UTC)[reply]

Thanks, Zefr — this framing works well and I agree it better reflects due weight for general readers. I appreciate the inclusion of the fructokinase ATP-consuming pathway while clarifying that its relevance is primarily under high-intake conditions.

My goal was simply to ensure that the biochemical mechanism itself was documented accurately in the biochemistry section, and I think this revision achieves that in a MED-compliant way.

Happy to support this wording. Potentialmotion (talk) 20:32, 9 January 2026 (UTC)[reply]

Under conditions of an ordinary diet with low levels of fructose consumed, uric acid production is negligible.^[1][2] When fructose consumption is excessive, uric acid levels can increase via an unregulated fructokinase pathway that consumes ATP and converts fructose into fructose-1-phosphate, leading to the degradation of AMP into uric acid.^[3] Other factors possibly contributing to increased risk of hyperuricemia include alcohol consumption, obesity, male sex, and aging.^[1]