Fructose Metabolism and Disease Mechanisms: From Nutritional Excess to Obesity and Multiorgan Pathophysiology.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic, animal, and clinical literature without systematic review methodology.
PubMed 41914164 · doi:10.31083/FBE46304
What was done
This narrative review synthesized current evidence from animal and human studies on the biochemical and molecular pathways linking excessive fructose consumption to obesity and multiorgan pathophysiology, focusing on mechanisms such as fructokinase C activation, ATP depletion, uric acid generation, oxidative stress, and inflammatory signaling pathways.
What was found
The abstract reports no quantitative data or effect sizes. It qualitatively summarizes that excess fructose metabolism induces hepatic steatosis, pancreatic beta-cell dysfunction, renal fibrosis, intestinal barrier disruption with dysbiosis, cardiometabolic impairment, pulmonary inflammation, and neurocognitive decline, framing fructose as an active metabolic disruptor rather than a simple caloric contributor.
Why it matters
It provides a broad framework linking dietary fructose overload to multiorgan damage through shared metabolic and inflammatory cascades.
Limits
As a narrative review, it does not use systematic search or selection protocols and pools diverse animal and human data without quantitative synthesis. No specific sample sizes, trial designs, or numerical risk estimates are provided in the abstract.
Cited by
- supports Uric acid is a downstream metabolite of fructose.