ArticleEndocrinology2019
Interactions Between the Gravitostat and the Fibroblast Growth Factor System for the Regulation of Body Weight.
Article in Endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06619028 (Effectiveness of the Use of External Body Weight in the Regulation of Body Weight, Body Composition and Analytical Parameters in Adults With Grade II and III Obesity), which is not on this map. Cited by 4 papers.
What it found
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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.
Effectiveness of the Use of External Body Weight in the Regulation of Body Weight, Body Composition and Analytical Parameters in Adults With Grade II and III Obesity
Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Trial
- The effect of increased weight loading on body weight is partly dependent on Piezo1 in osteoblast-lineage cells and TrkA signaling.Scientific reports · 2026Article
- A Body Weight Sensor Regulates Prepubertal Growth via the Somatotropic Axis in Male Rats.Endocrinology · 2021Article
- Increased weight loading reduces body weight and body fat in obese subjects - A proof of concept randomized clinical trial.EClinicalMedicine · 2020Article
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 at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both fibroblast growth factors (FGFs), by binding to FGF receptors (FGFRs), and activation of the gravitostat, by artificial loading, decrease the body weight (BW). Previous studies demonstrate that both the FGF system and loading have the capacity to regulate BW independently of leptin. The aim of the current study was to determine the possible interactions between the effect of increased loading and the FGF system for the regulation of BW. We observed that the BW-reducing effect of increased loading was abolished in mice treated with a monoclonal antibody directed against FGFR1c, suggesting interactions between the two systems. As serum levels of endocrine FGF21 and hepatic FGF21 mRNA were increased in the loaded mice compared with the control mice, we first evaluated the loading response in FGF21 over expressing mice with constant high FGF21 levels. Leptin treatment, but not increased loading, decreased the BW in the FGF21-overexpressing mice, demonstrating that specifically the loading effect is attenuated in the presence of high activity in the FGF system. However, as FGF21 knockout mice displayed a normal loading response on BW, FGF21 is neither mediating nor essential for the loading response. In conclusion, the BW-reducing effect of increased loading but not of leptin treatment is blocked by high activity in the FGF system. We propose that both the gravitostat and the FGF system regulate BW independently of leptin and that pharmacologically enhanced activity in the FGF system reduces the sensitivity of the gravitostat.
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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.