Evidence map›Paper›PMID 32652973›Full record

Trial reportBMC pregnancy and childbirth2020

Metformin and insulin treatment of gestational diabetes: effects on inflammatory markers and IGF-binding protein-1 - secondary analysis of a randomized controlled trial.

Mikael S Huhtala, Kristiina Tertti, Juuso Juhila, Timo Sorsa, Tapani Rönnemaa

Registry-linked trialOpen access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in BMC pregnancy and childbirth, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It reports registered trial NCT01240785. Cited by 9 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 3 pooled it
1.2field-weighted citation impact, top 16% 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.

NCT01240785 phase4completed

Metformin Versus Insulin in Gestational Diabetes. A Randomized Controlled Single Center Trial.

Ran2006Enrolled221Registered outcomes13Posted comparisons0ConditionsGestational DiabetesArmsInsulin, Metformin
Open the trial in the graph
3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 3 syntheses or guidelines pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Gestational weight gain according to treatment in gestational diabetes: a systematic review and meta-analysis.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2025
    Pooled it
  3. Pooled it
  4. Review
  5. Article
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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

5 authors at 3 institutions in 2 countries.

Mikael S HuhtalaDepartment of Obstetrics and Gynecology, University of Turku, 20014, Turku, Finland. misahu@utu.fi.ORCID https://orcid.org/0000-0001-5564-9788
Kristiina TerttiDepartment of Obstetrics and Gynecology, University of Turku, 20014, Turku, Finland.
Juuso JuhilaMedix Biochemica, Klovinpellontie 3, 02180, Espoo, Finland.
Timo SorsaDepartment of Oral and Maxillofacial Diseases, Head and Neck Center, University of Helsinki and Helsinki University Hospital, P.O. Box 63, 00014, Helsinki, Finland.
Tapani RönnemaaDepartment of Medicine, University of Turku, 20014, Turku, Finland.
University of Turku · FIUnited Medix Laboratories (Finland) · FIUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGestational diabetes mellitus (GDM) is characterized by disturbed glucose metabolism and activation of low-grade inflammation. We studied whether metformin treatment has favorable or unfavorable effects on inflammatory markers and insulin-like growth factor-binding protein 1 (IGFBP-1) in GDM patients compared with insulin, and whether these markers associate with major maternal or fetal clinical outcomes.

methodsThis is a secondary analysis of a previous randomized controlled trial comparing metformin (n = 110) and insulin (n = 107) treatment of GDM. Fasting serum samples were collected at the time of diagnosis (baseline, mean 30 gestational weeks [gw]) and at 36 gw. Inflammatory markers serum high-sensitivity CRP (hsCRP), interleukin-6 (IL-6), matrix metalloproteinase-8 (MMP-8) and glycoprotein acetylation (GlycA) as well as three IGFBP-1 phosphoisoform concentrations were determined.

resultsIn the metformin and insulin groups combined, hsCRP decreased (p = 0.01), whereas IL-6 (p = 0.002), GlycA (p < 0.0001) and all IGFBP-1 phosphoisoforms (p < 0.0001) increased from baseline to 36 gw. GlycA (p = 0.02) and non-phosphorylated IGFBP-1 (p = 0.008) increased more in patients treated with metformin than those treated with insulin. Inflammatory markers did not clearly associate with pregnancy outcomes but non-phosphorylated IGFBP-1 was inversely associated with gestational weight gain.

conclusionsMetformin had beneficial effects on maternal serum IGFBP-1 concentrations compared to insulin, as increased IGFBP-1 related to lower total and late pregnancy maternal weight gain. GlycA increased more during metformin treatment compared to insulin. The significance of this observation needs to be more profoundly examined in further studies. There were no evident clinically relevant relations between inflammatory markers and pregnancy outcome measures.

trial registrationThe trial comparing metformin and insulin treatment was registered in ClinicalTrials.gov ( NCT01240785 ) November 3, 2010. Retrospectively registered.

Indexed as

AdultBiomarkersBlood GlucoseDiabetes, GestationalFemaleHumansHypoglycemic AgentsInsulinInsulin-Like Growth Factor Binding Protein 1MetforminPregnancyPregnancy OutcomeYoung AdultBiomarkersBlood GlucoseHypoglycemic AgentsIGFBP1 protein, humanInsulinInsulin-Like Growth Factor Binding Protein 1MetforminGestational diabetesIGFBP-1Insulin-like growth factor-binding protein 1Low-grade inflammationMetformin

Identifiers

PMID32652973
PMCPMC7353798
OpenAlexW3042198205

What Socratic holds

Textmetadata
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.