Evidence map›Paper›PMID 26200703›Full record

ArticlePediatric research2015

Recurrent hypoinsulinemic hyperglycemia in neonatal rats increases PARP-1 and NF-κB expression and leads to microglial activation in the cerebral cortex.

Tate Gisslen, Kathleen Ennis, Vineet Bhandari, Raghavendra Rao

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Pediatric research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Association of hyperglycemia in extremely preterm infants with neurodevelopmental outcomes at 18 months of corrected age.Journal of perinatology : official journal of the California Perinatal Association · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Cerebral Effects of Neonatal Dysglycemia.Clinics in perinatology · 2022
    Review
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Article
  14. Diminished growth and lower adiposity in hyperglycemic very low birth weight neonates at 4 months corrected age.Journal of perinatology : official journal of the California Perinatal Association · 2016
    Observational
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 2 institutions in 1 country.

Tate GisslenDivision of Neonatology, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota.
Kathleen EnnisDivision of Neonatology, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota.
Vineet BhandariDepartment of Pediatrics (Neonatology) and Obstetrics, Gynecology, and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut.
Raghavendra RaoDivision of Neonatology, Department of Pediatrics, University of Minnesota, Minneapolis, Minnesota.
University of Minnesota · USYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHyperglycemia is a common metabolic problem in extremely low-birth-weight preterm infants. Neonatal hyperglycemia is associated with increased mortality and brain injury. Glucose-mediated oxidative injury may be responsible. Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme involved in DNA repair and cell survival. However, PARP-1 overactivation leads to cell death. NF-κB is coactivated with PARP-1 and regulates microglial activation. The effects of recurrent hyperglycemia on PARP-1/NF-κB expression and microglial activation are not well understood.

methodsRat pups were subjected to recurrent hypoinsulinemic hyperglycemia of 2 h duration twice daily from postnatal (P) day 3-P12 and killed on P13. mRNA and protein expression of PARP-1/NF-κB and their downstream effectors were determined in the cerebral cortex. Microgliosis was determined using CD11 immunohistochemistry.

resultsRecurrent hyperglycemia increased PARP-1 expression confined to the nucleus and without causing PARP-1 overactivation and cell death. NF-κB mRNA expression was increased, while IκB mRNA expression was decreased. inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), and neuronal nitric oxide synthase (nNOS) mRNA expressions were decreased. Hyperglycemia significantly increased the number of microglia.

conclusionRecurrent hyperglycemia in neonatal rats is associated with upregulation of PARP-1 and NF-κB expression and subsequent microgliosis but not neuronal cell death in the cerebral cortex.

Indexed as

AnimalsAnimals, NewbornBlood GlucoseCD11 AntigensCerebral CortexDisease Models, AnimalGlucoseHyperglycemiaI-kappa B ProteinsInsulinMicrogliaNF-kappa BNF-KappaB Inhibitor alphaNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIOctreotideBlood GlucoseCD11 AntigensGlucoseI-kappa B ProteinsInsulinNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, ratNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINos2 protein, ratNos3 protein, ratOctreotideParp1 protein, ratPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesRNA, Messenger

Identifiers

PMID26200703
OpenAlexW986677348

What OpenQuestion holds

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Registered trials

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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.