Evidence map›Paper›PMID 26646100›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2016

Developmental programming: interaction between prenatal BPA exposure and postnatal adiposity on metabolic variables in female sheep.

Almudena Veiga-Lopez, Jacob Moeller, Rohit Sreedharan, Kanakadurga Singer, Carey Lumeng, Wen Ye, Anthony Pease, Vasantha Padmanabhan

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  11. Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus.American journal of physiology. Endocrinology and metabolism · 2023
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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

8 authors at 2 institutions in 1 country.

Almudena Veiga-LopezDepartment of Pediatrics, University of Michigan, Ann Arbor, Michigan; Department of Animal Sciences, Michigan State University, East Lansing, Michigan;
Jacob MoellerDepartment of Pediatrics, University of Michigan, Ann Arbor, Michigan;
Rohit SreedharanDepartment of Pediatrics, University of Michigan, Ann Arbor, Michigan;
Kanakadurga SingerDepartment of Pediatrics, University of Michigan, Ann Arbor, Michigan;
Carey LumengDepartment of Pediatrics, University of Michigan, Ann Arbor, Michigan;ORCID http://orcid.org/0000-0003-0303-6204
Wen YeDepartment of Biostatistics, University of Michigan, Ann Arbor, Michigan; and.
Anthony PeaseDepartment of Small Animal Clinical Sciences, Michigan State University, East Lansing, Michigan.
Vasantha PadmanabhanDepartment of Pediatrics, University of Michigan, Ann Arbor, Michigan; vasantha@umich.edu.
University of Michigan · USMichigan State University · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Bisphenol-A and Reproductive DysfunctionR01ES016541 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PADMANABHAN, VASANTHA · 2009 to 2013
$2.0M
NIDDK NIH HHS P30 DK020572NIEHS NIH HHS R01 ES016541NIEHS NIH HHS R01-ES-016541
6 · The paper itself

Abstract

Among potential contributors for the increased incidence of metabolic diseases is the developmental exposure to endocrine-disrupting chemicals such as bisphenol A (BPA). BPA is an estrogenic chemical used in a variety of consumer products. Evidence points to interactions of BPA with the prevailing environment. The aim of this study was to assess the effects of prenatal exposure to BPA on postnatal metabolic outcomes, including insulin resistance, adipose tissue distribution, adipocyte morphometry, and expression of inflammatory markers in adipose tissue as well as to assess whether postnatal overfeeding would exacerbate these effects. Findings indicate that prenatal BPA exposure leads to insulin resistance in adulthood in the first breeder cohort (study 1), but not in the second cohort (study 2), which is suggestive of potential differences in genetic susceptibility. BPA exposure induced adipocyte hypertrophy in the visceral fat depot without an accompanying increase in visceral fat mass or increased CD68, a marker of macrophage infiltration, in the subcutaneous fat depot. Cohens effect size analysis found the ratio of visceral to subcutaneous fat depot in the prenatal BPA-treated overfed group to be higher compared with the control-overfed group. Altogether, these results suggest that exposure to BPA during fetal life at levels found in humans can program metabolic outcomes that lead to insulin resistance, a forerunner of type 2 diabetes, with postnatal obesity failing to manifest any interaction with prenatal BPA relative to insulin resistance and adipocyte hypertrophy.

Indexed as

Insulin ResistanceObesityPrenatal Exposure Delayed EffectsAdipocytes, WhiteAdiposityAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticBenzhydryl CompoundsBisphenol A CompoundsCD68 MoleculeEstrogens, Non-SteroidalFemaleGenetic Predisposition to DiseaseHypertrophyIntra-Abdominal FatAntigens, CDAntigens, Differentiation, MyelomonocyticBenzhydryl Compoundsbisphenol ABisphenol A CompoundsCD68 antigen, humanCD68 MoleculeEstrogens, Non-SteroidalPhenolsadipocytesbisphenol Adevelopment origins and toxicologyinflammationinsulin resistance

Identifiers

PMID26646100
PMCPMC4888526
OpenAlexW2289069921

What OpenQuestion holds

Textmetadata
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.