ArticleScientific reports2017
AMPK is not required for the effect of metformin on the inhibition of BMP6-induced hepcidin gene expression in hepatocytes.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Overview of Metformin and Neurodegeneration: A Comprehensive Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The anti-inflammatory effect of metformin: The molecular targets.Genes to cells : devoted to molecular & cellular mechanisms · 2024Review
- The gastrointestinal tract is a major source of the acute metformin-stimulated rise in GDF15.Scientific reports · 2024Article
- Exercise mimetics: harnessing the therapeutic effects of physical activity.Nature reviews. Drug discovery · 2021Review
- Iron at the Interface of Hepatocellular Carcinoma.International journal of molecular sciences · 2021Review
- BRAF Controls the Effects of Metformin on Neuroblast Cell Divisions inInternational journal of molecular sciences · 2020Article
- Targeting AMPK Signaling as a Neuroprotective Strategy in Parkinson's Disease.Journal of Parkinson's disease · 2018Review
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
The biguanide metformin is used for its antidiabetic effect for many years but how metformin acts remains poorly understood and controversial. AMP-activated protein kinase (AMPK), a protein kinase that plays a key role in maintaining energy homeostasis, is assumed to be one of the prime targets of metformin. However, since our demonstration that AMPK is not required for the beneficial effects of metformin on the control of glycemia, the list of AMPK-independent actions of metformin is rapidly increasing. Given the conflicting results on the effects of metformin we sought, using our genetic mouse models deficient in the catalytic subunits of AMPK, to determine whether this kinase is involved in the effects of metformin on the expression of the iron-regulatory hormone hepcidin, as recently proposed. Here we demonstrate, using different approaches, either isolated hepatocytes that lack AMPK, or direct AMPK activators, that, AMPK activation is not necessary for metformin to inhibit BMP6-induced hepcidin gene expression. These results may shed new lights on the increasingly recognized AMPK-independent metformin's molecular action, an important area of current research.
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Registered trials
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