ArticleJournal of lipid research2026
Tryptophan and polyamine metabolism dysregulation serves as an early marker of high-fat diet-induced glucose intolerance.
Article in Journal of lipid research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- SRM-Mediated Spermidine Synthesis Links Lipid Overload With AMPK Pathway to Regulate Hepatic Insulin Signaling and Gluconeogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A high-fat diet (HFD) induces metabolic dysfunction early, before the onset of the classic obese phenotype. However, understanding this early process remains limited, and potential diagnostic systems are still poorly investigated, particularly in childhood obesity. Continuous blood glucose monitoring was performed in mice to evaluate the early metabolic effects of HFD exposure. Metabolomic and transcriptomic analyses were conducted to characterize metabolic and transcriptional changes at various HFD feeding stages and investigate underlying mechanisms. Venn analysis was applied to identify metabolites specific to early HFD exposure. These metabolites were further compared with those detected in obese children to identify potential early warning biomarkers of obesity. Week 3 of HFD feeding was identified as a critical turning point in metabolic dysfunction in mice. Metabolomic profiling revealed that significant metabolic remodeling had occurred before glucose intolerance, particularly involving alterations in tryptophan metabolism, polyamine metabolism, and glycerophospholipid metabolism. Moreover, 54 HFD-specific metabolites were identified during this early stage. Further analysis identified serotonin, formiminoglutamate, inosine, and spermine as potential early warning biomarkers for HFD-induced obesity. Finally, transcriptomic profiling revealed early activation of interleukin-17A and type I interferon pathways, implicating immune involvement in metabolic perturbations. Early HFD exposure induces metabolic reprogramming before the onset of glucose intolerance. These_under_edi findings provide new insights into the mechanisms of diet-induced metabolic dysfunction and support the identification of potential biomarkers for early detection, particularly in childhood obesity. Early high-fat diet exposure induces metabolic reprogramming before glucose intolerance, characterized by alterations in tryptophan and polyamine metabolism and revealing candidate early biomarkers of obesity.
Indexed as
Identifiers
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.