ArticleInternational journal of obesity (2005)2025
High fat diet induces gastric production of fibroblast growth factor 23 (FGF23).
Article in International journal of obesity (2005), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA high fat diet (HFD) leads to lesions of the gastric epithelium and causes a proinflammatory environment. Fibroblast growth factor 23 (FGF23), a bone hormone, regulates renal phosphate and vitamin D metabolism. Under pathophysiological conditions production of FGF23 is stimulated. HFD feeding elevates serum FGF23 levels through inflammation.
objectiveWe aimed to investigate whether HFD feeding and obesity is associated with gastric FGF23 production.
methodsMice were fed a standard diet or HFD for 12 weeks (long-term) or 1 week (short-term), and the stomachs were then examined. Additionally, corpus specimens from patients with obesity, human umbilical vein endothelial cells (HUVECs), and normal human gastric epithelial cells (GES-1) were studied. FGF23 production was examined by qPCR and Western blotting, mucosal integrity assessed by fluorescence microscopy, and FGF23-expressing cells analyzed by immunohistochemistry.
resultsIn mice, HFD feeding up-regulated Fgf23 expression and FGF23 protein abundance in the proximal glandular stomach. FGF23-positive cells were detected in damaged glandular and interglandular areas representing mucus-like cells, endothelial cells of interconnected blood vessels or stromal endothelial cells and myofibroblasts. FGF23 expression was associated with impaired tissue integrity, immune cell infiltration and lipid deposition, with less pronounced mucosal changes upon short-term HFD feeding. Gastric FGF23 was also detectable in patients with obesity, mainly in endothelial cells of dilated and interconnected vessels. In HUVECs, pro-angiogenic adipokine leptin ramped up FGF23 transcript levels. In GES-1 cells, proinflammatory cytokine interleukin-1β (IL-1β) tended to enhance FGF23 expression.
conclusionsHFD feeding stimulates gastric FGF23 production and, in particular, increases the number of FGF23-expressing endothelial and epithelial cells.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.