Evidence map›Paper›PMID 31177313›Full record

ArticleDiabetologia2019

Augmented insulin secretory response in early pregnancy.

Camille E Powe, Larraine P Huston Presley, Joseph J Locascio, Patrick M Catalano

Open access · bronzeAbstract read
In one paragraph

Article in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% 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.

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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. The Double-Edged Sword of Gestational Insulin Resistance: Navigating Maternal Adaptation and Its Risks for Pregnancy and Offspring Health.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  5. Article
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  9. Exploring the Role of Kisspeptin in Polycystic Ovary Syndrome and Its Associated Pregnancy Complications.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
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8 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

4 authors at 4 institutions in 1 country.

Camille E PoweDiabetes Unit, Endocrine Division, Massachusetts General Hospital, 50 Staniford Street, Suite 301, Boston, MA, 02114, USA. camille.powe@mgh.harvard.edu.ORCID 0000-0002-7060-7778
Larraine P Huston PresleyDepartment of Reproductive Biology, Case Western Reserve University, MetroHealth Medical Center, Cleveland, OH, USA.
Joseph J LocascioAlzheimer's Disease Research Center, Neurology Dept, Massachusetts General Hospital, Boston, MA, USA.
Patrick M CatalanoMother Infant Research Institute, Department of Obstetrics and Gynecology, Tufts University School of Medicine, Boston, MA, USA.
Harvard University · USMassachusetts General Hospital · USMetroHealth Medical Center · USTufts University · US

Funding

The Harvard Clinical and Translational Science CenterUL1TR002541 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2018 to 2022
$93.0M
CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024989 · NCRR · CASE WESTERN RESERVE UNIVERSITY · PI DAVIS, PAMELA B · 2007 to 2011
$53.7M
Clinical and Translational Science Collaborative of ClevelandUL1TR002548 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI MCCOMSEY, GRACE A · 2018 to 2022
$35.5M
INSULIN RESISTANCE AND GLUCOSE METABOLISM IN PREGNANCYR01HD022965 · NICHD · CASE WESTERN RESERVE UNIVERSITY · PI CATALANO, PATRICK · 1994 to 2011
$2.3M
Elucidating Determinants of Gestational Beta-Cell Adaptation and FailureK23DK113218 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI POWE, CAMILLE ELISE · 2017 to 2021
$1.0M
NCATS NIH HHS UL1 TR002541NCATS NIH HHS UL1 TR002548NCRR NIH HHS UL1 RR024989NICHD NIH HHS R01 HD022965NIDDK NIH HHS K23 DK113218
6 · The paper itself

Abstract

aims/hypothesisThis study aimed to examine changes in the insulin secretory response in early pregnancy, while accounting for changes in insulin sensitivity.

methodsThis is a secondary analysis of a previously conducted longitudinal physiological study. In 34 women, insulin secretory response (by IVGTT) and insulin sensitivity (by euglycaemic clamp) were assessed prior to pregnancy, in early pregnancy (12-14 weeks gestation) and in late pregnancy (34-36 weeks gestation). Using mixed-effects models, we compared insulin secretory response and sensitivity in early pregnancy to the same variables prior to pregnancy and in late pregnancy, with adjustment for age, obesity status and gestational diabetes mellitus (GDM). We examined changes in insulin secretory response after adjustment for insulin sensitivity using both multivariate modelling and the disposition index (DI). We explored the relationship between insulin secretory response and circulating hormones.

resultsThe insulin secretory response increased from prior to pregnancy to early pregnancy (unadjusted mean [SD] first-phase insulin response 465.1 [268.5] to 720 [358.2], p < 0.0001) and from early pregnancy to late pregnancy (to 924 [494.6], p = 0.01). Insulin sensitivity increased from prior to pregnancy to early pregnancy (insulin sensitivity index 0.10 [0.04] to 0.12 [0.05], p = 0.001) and decreased in late pregnancy (to 0.06 [0.03], p < 0.0001). Accounting for changes in insulin sensitivity, using either multivariate modelling or the DI, did not attenuate the early-pregnancy augmentation of insulin secretory response. Leptin was positively associated with insulin secretory response, independent of insulin sensitivity and adiposity (p = 0.004). Adjustment for leptin attenuated the observed augmentation of insulin secretory response in early pregnancy (adjusted mean change 121.5, p = 0.13). CONCLUSIONS/

interpretationThe insulin secretory response increases markedly in early pregnancy, prior to and independent of changes in insulin sensitivity. Circulating hormones may mediate this metabolic adaptation. Identifying mediators of this physiological effect could have therapeutic implications for treating hyperglycaemia during and outside of pregnancy.

Indexed as

Pregnancy Trimester, FirstPregnancy Trimester, ThirdAdultAge FactorsBlood GlucoseBody Mass IndexCytokinesDiabetes, GestationalFemaleGlucose Tolerance TestHumansHyperinsulinismInsulinInsulin ResistanceLeptinLongitudinal StudiesBlood GlucoseCytokinesInsulinLeptinTumor Necrosis Factor-alphaGestational diabetesGlucose metabolismInsulin secretionPhysiologyPregnancy

Identifiers

PMID31177313
PMCPMC6786902
OpenAlexW2953822763

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.