Evidence map›Paper›PMID 21257748›Full record

ArticleThe Journal of biological chemistry2011

Inflammation of the hypothalamus leads to defective pancreatic islet function.

Vivian C Calegari, Adriana S Torsoni, Emerielle C Vanzela, Eliana P Araújo, Joseane Morari, Claudio C Zoppi, Lourenço Sbragia, Antonio C Boschero, Lício A Velloso

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

32 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Hypothalamic inflammation in obesity and metabolic disease.The Journal of clinical investigation · 2017
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Hypothalamic inflammation and gliosis in obesity.Current opinion in endocrinology, diabetes, and obesity · 2015
    Review
  15. Article
  16. Article
  17. Article
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  19. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 3 countries.

Vivian C CalegariLaboratory of Cell Signaling, of Campinas, 13084-970 Sao Paulo, Brazil.
Adriana S Torsoni
Emerielle C Vanzela
Eliana P Araújo
Joseane Morari
Claudio C Zoppi
Lourenço Sbragia
Antonio C Boschero
Lício A Velloso
Institute of Molecular Biology and Biophysics · RUToxicologie, Pharmacologie et Signalisation Cellulaire · FRUniversidade Estadual de Campinas (UNICAMP) · BRUniversidade de Ribeirão Preto · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus results from the complex association of insulin resistance and pancreatic β-cell failure. Obesity is the main risk factor for type 2 diabetes mellitus, and recent studies have shown that, in diet-induced obesity, the hypothalamus becomes inflamed and dysfunctional, resulting in the loss of the perfect coupling between caloric intake and energy expenditure. Because pancreatic β-cell function is, in part, under the control of the autonomic nervous system, we evaluated the role of hypothalamic inflammation in pancreatic islet function. In diet-induced obesity, the earliest markers of hypothalamic inflammation are present at 8 weeks after the beginning of the high fat diet; similarly, the loss of the first phase of insulin secretion is detected at the same time point and is restored following sympathectomy. Intracerebroventricular injection of a low dose of tumor necrosis factor α leads to a dysfunctional increase in insulin secretion and activates the expression of a number of markers of apoptosis in pancreatic islets. In addition, the injection of stearic acid intracerebroventricularly, which leads to hypothalamic inflammation through the activation of tau-like receptor-4 and endoplasmic reticulum stress, produces an impairment of insulin secretion, accompanied by increased expression of markers of apoptosis. The defective insulin secretion, in this case, is partially dependent on sympathetic signal-induced peroxisome proliferator receptor-γ coactivator Δα and uncoupling protein-2 expression and is restored after sympathectomy or following PGC1α expression inhibition by an antisense oligonucleotide. Thus, the autonomic signals generated in concert with hypothalamic inflammation can impair pancreatic islet function, a phenomenon that may explain the early link between obesity and defective insulin secretion.

Indexed as

AnimalsDiabetes Mellitus, Type 2Dietary FatsHypothalamic DiseasesHypothalamusInflammationInsulinInsulin SecretionIslets of LangerhansMaleObesityPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsRats, WistarRNA-Binding ProteinsStearic AcidsDietary FatsInsulinPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratRNA-Binding Proteinsstearic acidStearic AcidsTranscription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID21257748
PMCPMC3075634
OpenAlexW2066859044

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.