ReviewJournal of nutrition and metabolism2025
Mindful Eating: A Deep Insight Into Fructose Metabolism and Its Effects on Appetite Regulation and Brain Function.
Review in Journal of nutrition and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- On the Origin of the Brain Semi-Heavy Water Deuterium MR Signal Following Administration of Deuterated Metabolic Substrate: A Cautionary Tale.Magnetic resonance in medicine · 2026Article
- D-Fructose Exposure Impairs Neuronal Development in Mouse Neural Stem Cells.International journal of molecular sciences · 2026Article
- Fructose Intake Is Associated with Brain Metabolic Reprogramming and Exacerbation of Alzheimer-like Alterations in APP/PS1 Mice.International journal of molecular sciences · 2026Article
- Hijacking Sodium-Glucose Cotransporters: Fructose Drives Neuronal and Microglial Dysfunction.ASN neuro · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fructose, a common sweetener in modern diets, has profound effects on both metabolism and brain function, primarily due to its distinct metabolic pathways. Unlike glucose, fructose bypasses critical regulatory steps in metabolism, particularly the phosphofructokinase-1 (PFK-1) feedback inhibition, leading to uncontrolled metabolism and increased fat storage. This review delves into the metabolic consequences of fructose consumption, including its limited role in directly stimulating insulin secretion, which affects satiety signaling and contributes to increased food intake. The small intestine initially helps metabolize ingested fructose, shielding the liver and brain from excessive exposure. However, when consumed in excess, particularly in diets high in processed foods, this protective mechanism becomes overwhelmed, contributing to metabolic disorders such as insulin resistance, obesity, and fatty liver disease. The review also explores fructose's impact on the brain, with a focus on the hippocampus, a key region for memory and learning. Chronic high fructose intake has been linked to mitochondrial dysfunction, increased production of reactive oxygen species (ROS), and neuroinflammation, all of which contribute to cognitive decline and impairments in memory and learning. Additionally, fructose-induced alterations in insulin signaling in the brain are associated with increased risk for neurodegenerative diseases. These findings underscore the potential long-term neurological consequences of excessive fructose intake and highlight the need for further human studies to assess the full spectrum of its effects on brain health. Addressing the rising consumption of fructose, particularly in processed foods, is essential for developing targeted strategies to mitigate its adverse metabolic and cognitive outcomes.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.