Evidence map›Paper›PMID 16902066›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2006

Metformin increases the PGC-1alpha protein and oxidative enzyme activities possibly via AMPK phosphorylation in skeletal muscle in vivo.

Masataka Suwa, Toru Egashira, Hiroshi Nakano, Haruka Sasaki, Shuzo Kumagai

Registry-linked trialAbstract read
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In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00536211 (Physical Inactivity and Insulin Resistance in Skeletal Muscle.), which is not on this map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

NCT00536211 nawithdrawnstarted 2009, after this paper: background citation

Physical Inactivity and Insulin Resistance in Skeletal Muscle.

Ran2009Enrolled0Registered outcomes2Posted comparisons0ConditionsHypercholesterolemia, Hypertension, Insulin Resistance, Metabolic Syndrome XArmsExercise, Metformin
Open the trial in the graph
3 · Its place in the literature

Who cites it

106 citing papers in PubMed, 206 citations in OpenAlex.

  1. Trial
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  4. Metformin Partially Attenuates Simvastatin-Induced Myotoxic Responses in C2C12 Myotubes Through Metabolic Adaptation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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46 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Masataka SuwaInstitute of Health Science, Kyushu University, Kasuga, Fukuoka 816-8580, Japan. suwa-m@students.ihs.kyushu-u.ac.jp
Toru Egashira
Hiroshi Nakano
Haruka Sasaki
Shuzo Kumagai
Kyushu University · JPFukuoka University · JPNakamura Gakuen University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK), which was activated by an antihyperglycemic drug metformin, has been hypothesized to mediate metabolic adaptations. The purposes of the present study were 1) to confirm whether acute metformin administration induced AMPK phosphorylation and 2) to determine whether chronic metformin treatment increased the peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) protein expression, glycolytic and oxidative enzyme activities, and cytochrome c and glucose transporter-4 (GLUT4) protein expressions in the rat soleus and red and white gastrocnemius muscles. The single oral administration of metformin (300 mg/kg body wt) enhanced the AMPK phosphorylation at 5 and/or 6 h after treatment. In the chronic study, rats were fed either normal chow or chow containing 1% metformin for 14 days. Metformin treatment resulted in a mean daily metformin intake of 631 mg.kg body wt(-1).day(-1). Metformin increased the PGC-1alpha content in all three muscles. Metformin increased the hexokinase activity in the white gastrocnemius, the citrate synthase activity in all three muscles, and the beta-hydroxyacyl-CoA dehydrogenase activity in the soleus. The cytochrome c protein content in the soleus muscle also increased. The GLUT4 content was unchanged by metformin. These results suggest that metformin enhances the PGC-1alpha expression and mitochondrial biogenesis possibly at least in part via AMPK phosphorylation in the skeletal muscle. Metformin has thus been proposed to possibly ameliorate insulin resistance, at least partially, by means of such metabolic effects.

Indexed as

Administration, OralAMP-Activated Protein KinasesAnimalsEnzyme ActivationGlucose Transporter Type 4GlycolysisMaleMetabolic Clearance RateMetforminMultienzyme ComplexesMuscle, SkeletalOxidation-ReductionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhosphorylationProtein Serine-Threonine KinasesRatsAMP-Activated Protein KinasesGlucose Transporter Type 4MetforminMultienzyme ComplexesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratProtein Serine-Threonine KinasesRNA-Binding ProteinsSlc2a4 protein, ratTranscription Factors

Identifiers

PMID16902066
OpenAlexW2101579318

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.