Evidence mapPaperPMID 25017630Full record

ArticleThe Biochemical journal2014

Effects of metformin and other biguanides on oxidative phosphorylation in mitochondria.

Hannah R Bridges, Andrew J Y Jones, Michael N Pollak, Judy Hirst

Registry-linked trialOpen access · hybridFull text read
In one paragraph

Article in The Biochemical journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03031821 (A Randomized Phase 3 Trial of Metformin in Patients Initiating Androgen Deprivation Therapy as Prevention and Intervention of Metabolic Syndrome), which is not on this map. Cited by 381 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
381citing papers in PubMed, 1 pooled it
19.2field-weighted citation impact, top 1% 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.

NCT03031821 phase3terminatedstarted 2018, after this paper: background citation

A Randomized Phase 3 Trial of Metformin in Patients Initiating Androgen Deprivation Therapy as Prevention and Intervention of Metabolic Syndrome: The Prime Study

Ran2018Enrolled166Registered outcomes30Posted comparisons0ConditionsMetabolic Syndrome, Prostate CancerArmsMetformin, Placebo Oral Tablet
Open the trial in the graph
3 · Its place in the literature

Who cites it

381 citing papers in PubMed, 1 synthesis or guideline pooled it, 637 citations in OpenAlex.

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321 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Hannah R Bridges*Medical Research Council Mitochondrial Biology Unit, Wellcome Trust/MRC Building, Hills Road, Cambridge, CB2 0XY, U.K.
Andrew J Y Jones*Medical Research Council Mitochondrial Biology Unit, Wellcome Trust/MRC Building, Hills Road, Cambridge, CB2 0XY, U.K.
Michael N Pollak†Department of Oncology, McGill University and Lady Davis Research Institute of the Jewish General Hospital, Montreal, Quebec, Canada, H3T 1E2.
Judy Hirst*Medical Research Council Mitochondrial Biology Unit, Wellcome Trust/MRC Building, Hills Road, Cambridge, CB2 0XY, U.K.
Jewish General Hospital · CA

Funding

CIHRMedical Research Council MC_U105663141Medical Research Council U105663141
6 · The paper itself

Abstract

The biguanide metformin is widely prescribed for Type II diabetes and has anti-neoplastic activity in laboratory models. Despite evidence that inhibition of mitochondrial respiratory complex I by metformin is the primary cause of its cell-lineage-specific actions and therapeutic effects, the molecular interaction(s) between metformin and complex I remain uncharacterized. In the present paper, we describe the effects of five pharmacologically relevant biguanides on oxidative phosphorylation in mammalian mitochondria. We report that biguanides inhibit complex I by inhibiting ubiquinone reduction (but not competitively) and, independently, stimulate reactive oxygen species production by the complex I flavin. Biguanides also inhibit mitochondrial ATP synthase, and two of them inhibit only ATP hydrolysis, not synthesis. Thus we identify biguanides as a new class of complex I and ATP synthase inhibitor. By comparing biguanide effects on isolated complex I and cultured cells, we distinguish three anti-diabetic and potentially anti-neoplastic biguanides (metformin, buformin and phenformin) from two anti-malarial biguanides (cycloguanil and proguanil): the former are accumulated into mammalian mitochondria and affect oxidative phosphorylation, whereas the latter are excluded so act only on the parasite. Our mechanistic and pharmacokinetic insights are relevant to understanding and developing the role of biguanides in new and existing therapeutic applications, including cancer, diabetes and malaria.

Indexed as

AnimalsAntimalarialsAntineoplastic AgentsBiguanidesCattleDiabetes Mellitus, Type 2Electron Transport Complex IHep G2 CellsHumansMetforminMitochondria, HeartMitochondria, LiverMitochondrial Proton-Translocating ATPasesOxidative PhosphorylationPlasmodiumProguanilAntimalarialsAntineoplastic AgentsBiguanidescycloguanilElectron Transport Complex IMetforminMitochondrial Proton-Translocating ATPasesProguanilTriazines

Identifiers

PMID25017630
PMCPMC4148174
OpenAlexW2012442095

What Socratic holds

Textfull text, public
LicenceCC BY
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 Socratic graph.