Trial reportPloS one2014

Novel gut-based pharmacology of metformin in patients with type 2 diabetes mellitus.

Antonella Napolitano, Sam Miller, Andrew W Nicholls, David Baker, Stephanie Van Horn, Elizabeth Thomas, Deepak Rajpal, Aaron Spivak, James R Brown, Derek J Nunez

Erratum issued Registry-linked trialOpen access · goldFull text readClinical TrialMulticenter Study
In one paragraph

Trial report in PloS one, 2014. The graph read 2 numbers from its abstract, feeding 2 cells of the map: it . An erratum has been issued. It reports registered trial NCT01357876. Cited by 151 papers, 6 of them syntheses that pooled it.

2numbers the graph read from it
1cell of the map it votes in
151citing papers in PubMed, 6 pooled it
10.8field-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.

← favours the treatmentfavours the comparator →
-21.00 · no effect
Glycemic controlfavours the treatment · head-to-head · t2dfeeds one cell of the map
decrease -21.0p<0.0001
The plasma glucose concentrations were decreased by ∼21% (p<0.0001) from Visit 3 to Visit 4 when fasting CBG had returned to baseline levels following the reintroduction of metformin.

Read, but not usablea number the graph found but could not read as for or against

Adverse events & safetydescribes a change within one group, not a comparison · head-to-head · t2dfeeds one cell of the map
ls increase 15.0p = 0.0006
Following metformin withdrawal at Visit 1, the 12-hour mean venous plasma glucose levels increased by ∼15% (p = 0.0006) from baseline to Visit 3 when fasting CBG had increased by ∼25%.

clause the extractor read what became the number

2 · Its place on the map

Where it lands on the map

Rows are treatments, columns are outcomes. The coloured squares are the cells this paper feeds, coloured by the vote it casts there. Click one to jump to what this paper adds to it.

supports the treatmentfavours the comparatorno clear differenceread, but no usable result
3 · What it changes

What it adds to each cell

For every cell the paper feeds: the belief in the claim with and without this paper, and this paper's estimate drawn against every other readable study in the cell. The ringed dot is this paper.

Metformin×glycemic control

No readable resultOpen on the map →What to test next →

40 readable studies in this cell: 41 favour the treatment, 12 find no difference, 8 favour the comparator.

Belief with this paper
0.84replicated · 32 families support, 6 contradict · against placebo
Without itNot a counted family in this claim, so removing it changes nothing.
← favours the treatmentfavours the comparator →
0 · no effect
This paper8 enrolled · 2010
decrease -21.0
NCT017190031,413 enrolled · 2012
Adjusted mean -0.72-0.95 to -0.48
NCT018093271,186 enrolled · 2013
Δ -0.40-0.59 to -0.21
NCT022730501,136 enrolled · 2014
Δ -0.89-1.08 to -0.69
NCT008598981,093 enrolled · 2009
Δ -0.53-0.74 to -0.32
Δ -0.85-43.8 to 26.7
NCT00643851994 enrolled · 2008
Δ -0.86-1.11 to -0.62
NCT01708902876 enrolled · 2012
Δ -1.00-1.23 to -0.78
NCT00676338820 enrolled · 2008
Δ -0.05-0.26 to 0.17
NCT01126580807 enrolled · 2010
Δ -0.22-0.36 to -0.08
NCT01023581784 enrolled · 2009
Δ -0.67-0.96 to -0.37
NCT01076088744 enrolled · 2010
Δ -0.84-1.15 to -0.52
NCT00386100688 enrolled · 2006
Δ -0.49-0.67 to -0.30

Metformin×adverse events & safety

No readable resultOpen on the map →What to test next →

22 readable studies in this cell: 9 favour the treatment, 8 find no difference, 5 favour the comparator.

Belief with this paper
0.27contested · 4 families support, 11 contradict · against placebo
Without itNot a counted family in this claim, so removing it changes nothing.
← favours the treatmentfavours the comparator →
0 · no effect
NCT017190031,413 enrolled · 2012
Adjusted mean -0.72-0.95 to -0.48
NCT018093271,186 enrolled · 2013
Δ -0.40-0.59 to -0.21
NCT022730501,136 enrolled · 2014
Δ -8.90-13.3 to -4.50
NCT01126580807 enrolled · 2010
Δ -0.22-0.36 to -0.08
NCT01023581784 enrolled · 2009
Δ -0.67-0.96 to -0.37
NCT00386100688 enrolled · 2006
Δ 1.47-14.8 to 20.8
NCT01217073685 enrolled · 2010
Δ 1.00-9.80 to 13.1
NCT01890122647 enrolled · 2013
Δ -0.68-0.89 to -0.47
NCT00727857600 enrolled · 2007
Δ 0.860.51 to 1.22
NCT01958671461 enrolled · 2013
Δ -2.60-13.1 to 8.10
NCT00328172302 enrolled · 2006
Δ -0.85-1.10 to -0.59
NCT01485614200 enrolled · 2012
Δ 2.40-10.0 to 14.9

This paper's own estimate is on a different scale from the rest of the cell, so it is not drawn here.

4 · 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.

NCT01357876 phase1completed

Effect of Metformin on Gut Peptides , Bile Acids and Lipid Profiles in Type 2 Diabetics

Ran2010Enrolled8Registered outcomes5Posted comparisons0ConditionsDiabetes Mellitus, Type 2ArmsMetformin
Open the trial in the graph
5 · Its place in the literature

Who cites it

151 citing papers in PubMed, 6 syntheses or guidelines pooled it, 282 citations in OpenAlex.

  1. Pooled it
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91 more citing papers are in PubMed but not listed here.

6 · The record

Corrections and comments

  • Erratum issued
7 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Antonella NapolitanoImmuno-Inflammation Unit, GSK R&D, Stevenage, Herts, United Kingdom.
Sam MillerQuantitative Sciences, GSK R&D, Stevenage, Herts, United Kingdom.
Andrew W NichollsSafety Assessment, GSK R&D, Ware, Herts, United Kingdom.
David BakerSafety Assessment, GSK R&D, Ware, Herts, United Kingdom.
Stephanie Van HornTarget and Pathways Validation, GSK R&D, Upper Providence, Pennsylvania, United States of America.
Elizabeth ThomasTarget and Pathways Validation, GSK R&D, Upper Providence, Pennsylvania, United States of America.
Deepak RajpalComputational Biology, GSK R&D, Upper Providence, Pennsylvania, United States of America.
Aaron SpivakComputational Biology, GSK R&D, Upper Providence, Pennsylvania, United States of America.
James R BrownComputational Biology, GSK R&D, Upper Providence, Pennsylvania, United States of America.
Derek J NunezEnteroendocrine Discovery Unit, GlaxoSmithKline R&D, GSK R&D, Research Triangle Park, North Carolina, United States of America.
Providence College · USAge UK · GBGlaxoSmithKline (United States) · USPathways Behavioral Services · US

Funding

No grant is acknowledged in the PubMed record.

8 · The paper itself

Abstract

The marked sentences are the ones the graph read a number from.

unlabelledMetformin, a biguanide derivate, has pleiotropic effects beyond glucose reduction, including improvement of lipid profiles and lowering microvascular and macrovascular complications associated with type 2 diabetes mellitus (T2DM). These effects have been ascribed to adenosine monophosphate-activated protein kinase (AMPK) activation in the liver and skeletal muscle. However, metformin effects are not attenuated when AMPK is knocked out and intravenous metformin is less effective than oral medication, raising the possibility of important gut pharmacology. We hypothesized that the pharmacology of metformin includes alteration of bile acid recirculation and gut microbiota resulting in enhanced enteroendocrine hormone secretion. In this study we evaluated T2DM subjects on and off metformin monotherapy to characterize the gut-based mechanisms of metformin. Subjects were studied at 4 time points: (i) at baseline on metformin, (ii) 7 days after stopping metformin, (iii) when fasting blood glucose (FBG) had risen by 25% after stopping metformin, and (iv) when FBG returned to baseline levels after restarting the metformin. At these timepoints we profiled glucose, insulin, gut hormones (glucagon-like peptide-1 (GLP-1), peptide tyrosine-tyrosine (PYY) and glucose-dependent insulinotropic peptide (GIP) and bile acids in blood, as well as duodenal and faecal bile acids and gut microbiota. We found that metformin withdrawal was associated with a reduction of active and total GLP-1 and elevation of serum bile acids, especially cholic acid and its conjugates. These effects reversed when metformin was restarted. Effects on circulating PYY were more modest, while GIP changes were negligible. Microbiota abundance of the phylum Firmicutes was positively correlated with changes in cholic acid and conjugates, while Bacteroidetes abundance was negatively correlated. Firmicutes and Bacteroidetes representation were also correlated with levels of serum PYY. Our study suggests that metformin has complex effects due to gut-based pharmacology which might provide insights into novel therapeutic approaches to treat T2DM and associated metabolic diseases.

trial registrationwww.ClinicalTrials.gov NCT01357876.

Indexed as

Hypoglycemic AgentsIntestinal MucosaIntestinesMetforminAdolescentAdultAgedBile Acids and SaltsBlood GlucoseDiabetes Mellitus, Type 2FemaleGlucagon-Like Peptide 1HumansMaleMicrobiotaMiddle AgedBile Acids and SaltsBlood GlucoseGlucagon-Like Peptide 1Hypoglycemic AgentsMetforminPeptide YY

Identifiers

PMID24988476
PMCPMC4079657
OpenAlexW2092328954

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.