Evidence mapPaperPMID 37694284Full record

ArticleAmerican journal of physiology. Cell physiology2023

Redox state and altered pyruvate metabolism contribute to a dose-dependent metformin-induced lactate production of human myotubes.

Jennifer Maurer, Xinjie Zhao, Martin Irmler, Anders Gudiksen, Nanna S Pilmark, Qi Li, Thomas Goj, Johannes Beckers, Martin Hrabě de Angelis, Andreas L Birkenfeld and 6 more

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
field-weighted citation impact
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
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  3. Review
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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

16 authors.

Jennifer MaurerDepartment for Diagnostic Laboratory Medicine, Institute for Clinical Chemistry and Pathobiochemistry, University Hospital Tübingen, Tübingen, Germany.
Xinjie ZhaoKey Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, The Chinese Academy of Sciences, Dalian, China.
Martin IrmlerInstitute of Experimental Genetics, Helmholtz Munich, Neuherberg, Germany.
Anders GudiksenSection for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0003-1800-4838
Nanna S PilmarkCentre for Physical Activity Research (CFAS), Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark.
Qi LiKey Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, The Chinese Academy of Sciences, Dalian, China.
Thomas GojDepartment for Diagnostic Laboratory Medicine, Institute for Clinical Chemistry and Pathobiochemistry, University Hospital Tübingen, Tübingen, Germany.
Johannes BeckersInstitute of Experimental Genetics, Helmholtz Munich, Neuherberg, Germany.ORCID 0000-0001-7874-3822
Martin Hrabě de AngelisInstitute of Experimental Genetics, Helmholtz Munich, Neuherberg, Germany.ORCID 0000-0002-7898-2353
Andreas L BirkenfeldGerman Center for Diabetes Research (DZD), Neuherberg, Germany.
Andreas PeterDepartment for Diagnostic Laboratory Medicine, Institute for Clinical Chemistry and Pathobiochemistry, University Hospital Tübingen, Tübingen, Germany.ORCID 0000-0001-5732-2287
Rainer LehmannDepartment for Diagnostic Laboratory Medicine, Institute for Clinical Chemistry and Pathobiochemistry, University Hospital Tübingen, Tübingen, Germany.ORCID 0000-0003-1218-6810
Henriette PilegaardSection for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Kristian KarstoftCentre for Physical Activity Research (CFAS), Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark.ORCID 0000-0002-6596-4199
Guowang XuKey Laboratory of Separation Science for Analytical Chemistry, Dalian Institute of Chemical Physics, The Chinese Academy of Sciences, Dalian, China.ORCID 0000-0003-4298-3554
Cora WeigertDepartment for Diagnostic Laboratory Medicine, Institute for Clinical Chemistry and Pathobiochemistry, University Hospital Tübingen, Tübingen, Germany.ORCID 0000-0003-0358-776X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metformin-induced glycolysis and lactate production can lead to acidosis as a life-threatening side effect, but slight increases in blood lactate levels in a physiological range were also reported in metformin-treated patients. However, how metformin increases systemic lactate concentrations is only partly understood. Because human skeletal muscle has a high capacity to produce lactate, the aim was to elucidate the dose-dependent regulation of metformin-induced lactate production and the potential contribution of skeletal muscle to blood lactate levels under metformin treatment. This was examined by using metformin treatment (16-776 μM) of primary human myotubes and by 17 days of metformin treatment in humans. As from 78 µM, metformin induced lactate production and secretion and glucose consumption. Investigating the cellular redox state by mitochondrial respirometry, we found metformin to inhibit the respiratory chain complex I (776 µM,

Indexed as

Lactic AcidMetforminHumansLactate DehydrogenasesMuscle Fibers, SkeletalNADOxidation-ReductionOxidoreductasesPyruvatesLactate DehydrogenasesLactic AcidMetforminNADOxidoreductasesPyruvateslactatemetforminpyruvate dehydrogenase complexrespirationskeletal muscle

Identifiers

PMID37694284
PMCPMC10635655

What Socratic holds

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Registered trials

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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.