ReviewMolecular biology reports2026
The role of fibroblast growth factor 21 in diabetes and metabolic dysfunction.
Review in Molecular biology reports, 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.
- Exercise-Induced Hepatic Mitochondrial Reprogramming Across Muscle-Gut-Thyroid Axes in MASLD/MASH.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 21 (FGF21) is an endocrine hormone central to metabolic regulation under nutritional and cellular stress. Predominantly synthesized by the liver, FGF21 exerts pleiotropic effects through fibroblast growth factor receptor 1c (FGFR1c) and its co receptor β-Klotho, targeting adipose tissue, skeletal muscle, pancreas, and the central nervous system. In diabetes mellitus, FGF21 enhances insulin sensitivity, stimulates adiponectin secretion, alleviates hepatic steatosis, and protects pancreatic β-cells from oxidative and endoplasmic reticulum stress. These effects are mediated via key molecular pathways, including AMPK, SIRT1, PGC-1α, and mTOR signaling. Interestingly, despite elevated circulating FGF21 levels in obesity and type 2 diabetes, biological responsiveness is diminished-a phenomenon termed FGF21 resistance, characterised by impaired receptor expression, inflammatory signaling interference, and downstream signaling deficits. This review presents an in depth mechanistic overview of FGF21 signaling, its regulatory networks, and implications for glucose and lipid homeostasis, inflammation, mitochondrial health, and autophagy. Additionally, it discusses the development of pharmacologically optimized FGF21 analogs and multi agonists designed to overcome resistance and enhance therapeutic efficacy. As our comprehension of FGF21 biology deepens, elucidation of its molecular processes, resistance phenomena, and pharmacological refinement will be crucial in establishing FGF21 as a fundamental element of precision medicine for metabolic illnesses. The incorporation of FGF21 based strategies with combinatorial pharmacotherapy and tissue targeted delivery methods offers a potential approach to tackle the complicated pathophysiology of diabetes and improve clinical outcomes in affected populations.
Indexed as
Identifiers
42313341What 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.