Evidence map›Paper›PMID 26740602›Full record

ArticleDiabetes2016

Proximity to Delivery Alters Insulin Sensitivity and Glucose Metabolism in Pregnant Mice.

Barbara Musial, Denise S Fernandez-Twinn, Owen R Vaughan, Susan E Ozanne, Peter Voshol, Amanda N Sferruzzi-Perri, Abigail L Fowden

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
8.5field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Distinct macronutrient ratios optimize offspring survival, growth, and maternal glucose tolerance across mouse reproduction.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

7 authors at 1 institution in 1 country.

Barbara MusialDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, U.K.
Denise S Fernandez-TwinnUniversity of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, U.K.
Owen R VaughanDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, U.K.
Susan E OzanneUniversity of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, U.K.
Peter VosholUniversity of Cambridge Metabolic Research Laboratories, MRC Metabolic Disease Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, U.K.
Amanda N Sferruzzi-PerriDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, U.K.
Abigail L FowdenDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, U.K. alf100@cam.ac.uk.
University of Cambridge · GB

Funding

British Heart Foundation FS/09/029/27902Medical Research Council G0600717Medical Research Council MC_UU_12012/4Medical Research Council MC_UU_12012/5
6 · The paper itself

Abstract

In late pregnancy, maternal insulin resistance occurs to support fetal growth, but little is known about insulin-glucose dynamics close to delivery. This study measured insulin sensitivity in mice in late pregnancy at day 16 (D16) and near term at D19. Nonpregnant (NP) and pregnant mice were assessed for metabolite and hormone concentrations, body composition by DEXA, tissue insulin signaling protein abundance by Western blotting, glucose tolerance and utilization, and insulin sensitivity using acute insulin administration and hyperinsulinemic-euglycemic clamps with [(3)H]glucose infusion. Whole-body insulin resistance occurred in D16 pregnant dams in association with basal hyperinsulinemia, insulin-resistant endogenous glucose production, and downregulation of several proteins in hepatic and skeletal muscle insulin signaling pathways relative to NP and D19 values. Insulin resistance was less pronounced at D19, with restoration of NP insulin concentrations, improved hepatic insulin sensitivity, and increased abundance of hepatic insulin signaling proteins. At D16, insulin resistance at whole-body, tissue, and molecular levels will favor fetal glucose acquisition, while improved D19 hepatic insulin sensitivity will conserve glucose for maternal use in anticipation of lactation. Tissue sensitivity to insulin, therefore, alters differentially with proximity to delivery in pregnant mice, with implications for human and other species.

Indexed as

AnimalsDelivery, ObstetricFemaleGlucoseInsulin ResistanceLipid MetabolismMaleMiceMice, Inbred C57BLParturitionPregnancyTime FactorsGlucose

Identifiers

PMID26740602
PMCPMC4876930
OpenAlexW2232263866

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.