ArticleBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine2026
Vanadium(IV)-chlorodipicolinate alleviates hepatic steatosis via the AMPK/PGC-1α/CPT1a axis.
Article in Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine, 2026. 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
7 authors.
Funding
Abstract
Non-alcoholic fatty liver disease (NAFLD) is closely associated with type 2 diabetes mellitus, which is characterized by hepatic steatosis. Vanadium compounds have the potential to prevent hyperlipidemia. However, whether vanadium compound supplementation could rescue hepatic steatosis in NAFLD remains uncertain. We sought to investigate the molecular mechanisms by which vanadium(IV)-chlorodipicolinate (VOdipic-Cl) ameliorated hepatic steatosis in obesity. The therapeutic effect of VOdipic-Cl was evaluated using high-fat diet (HFD)-induced C57BL/6 mice and palmitic acid/oleic acid (PO)-treated L02 hepatocytes, respectively. Lipidomic analysis, RNA-sequencing (RNA-seq), Western blotting, and molecular dynamics simulation were employed to elucidate the molecular mechanism of VOdipic-Cl in regulating lipid metabolism in liver and hepatocytes. VOdipic-Cl treatment effectively reduced hepatic lipid accumulation and improved hepatic function in HFD-fed mice. Lipidomic analysis showed that the primary differential lipid metabolites were mainly associated with glycerophospholipid metabolism pathway. Transcriptomic analysis revealed that adenosine monophosphate-activated protein kinase (AMPK) signaling pathway was involved in the regulation of hepatic lipid metabolism by VOdipic-Cl treatment. Moreover, VOdipic-Cl-induced AMPK activation significantly restored hepatic mitochondrial homeostasis and reduced lipid accumulation through upregulating transcription factor peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and carnitine palmitoyltransferase 1 (CPT1) in hepatocytes, respectively. Our findings suggest that VOdipic-Cl triggers the activation of AMPK, leading to the upregulation of PGC-1α and CPT1 expression, ultimately improving mitochondrial homeostasis and decreasing lipid accumulation. Collectively, these molecular cascades contribute to the ameliorating effect of VOdipic-Cl on HFD-induced hepatic steatosis. This study also provides evidence supporting the potential utilization of VOdipic-Cl for the treatment of NAFLD.
Indexed as
Identifiers
42228233What 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.