Evidence map›Paper›PMID 24408314›Full record

ArticleDiabetes2014

Neutralizing Th2 inflammation in neonatal islets prevents β-cell failure in adult IUGR rats.

Lane J Jaeckle Santos, Changhong Li, Paschalis-Thomas Doulias, Harry Ischiropoulos, G Scott Worthen, Rebecca A Simmons

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
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  6. Neonatal IL-4 exposure decreases adipogenesis of male rats into adulthood.American journal of physiology. Endocrinology and metabolism · 2021
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  12. Transgenerational effects of maternal bisphenol: a exposure on offspring metabolic health.Journal of developmental origins of health and disease · 2019
    Article
  13. Article
  14. Fetal undernutrition, placental insufficiency, and pancreatic β-cell development programming in utero.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Review
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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

6 authors at 2 institutions in 1 country.

Lane J Jaeckle SantosDivision of Neonatology, Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Changhong Li
Paschalis-Thomas Doulias
Harry Ischiropoulos
G Scott Worthen
Rebecca A Simmons
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · US

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI MITCHELL A. LAZAR · 1986 to 2026
$48.3M
MECHANISMS BY WHICH IUGR LEADS TO DIABETESR01DK055704 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SIMMONS, REBECCA A · 2000 to 2014
$3.6M
CXC Chemokines and Regulation of GranulopoiesisR01AI099479 · NIAID · CHILDREN'S HOSP OF PHILADELPHIA · PI WORTHEN, GEORGE SCOTT · 2013 to 2017
$2.1M
Chemokine Compartmentalization and Neutrophil Accumulation in the LungR01HL105834 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI WORTHEN, GEORGE SCOTT · 2011 to 2014
$1.6M
Training Program in Genome-Environment Interactions in Neonatal DiseaseT32HD060556 · NICHD · CHILDREN'S HOSP OF PHILADELPHIA · PI WORTHEN, GEORGE SCOTT · 2010 to 2014
$922k
NHLBI NIH HHS R01 HL105834NIAID NIH HHS R01 AI099479NICHD NIH HHS 1T32-HD-060556NICHD NIH HHS 5T32-HD-00730525NICHD NIH HHS T32 HD060556NIDDK NIH HHS P30 DK019525NIDDK NIH HHS P30-DK-19525NIDDK NIH HHS R01 DK055704NIDDK NIH HHS R01-DK-055704
6 · The paper itself

Abstract

Intrauterine growth restriction (IUGR) leads to development of type 2 diabetes (T2D) in adulthood. The mechanisms underlying this phenomenon have not been fully elucidated. Inflammation is associated with T2D; however, it is unknown whether inflammation is causal or secondary to the altered metabolic state. Here we show that the mechanism by which IUGR leads to the development of T2D in adulthood is via transient recruitment of T-helper 2 (Th) lymphocytes and macrophages in fetal islets resulting in localized inflammation. Although this immune response is short-lived, it results in a permanent reduction in islet vascularity and impaired insulin secretion. Neutralizing interleukin-4 antibody therapy given only in the newborn period ameliorates inflammation and restores vascularity and β-cell function into adulthood, demonstrating a novel role for Th2 immune responses in the induction and progression of T2D. In the neonatal stage, inflammation and vascular changes are reversible and may define an important developmental window for therapeutic intervention to prevent adult-onset diabetes.

Indexed as

AnimalsAnimals, NewbornAntibodies, NeutralizingFetal Growth RetardationInflammationInsulin-Secreting CellsInterleukin-4Islets of LangerhansRatsTh2 CellsAntibodies, NeutralizingInterleukin-4

Identifiers

PMID24408314
PMCPMC3994952
OpenAlexW2162863886

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.