Evidence map›Paper›PMID 22315324›Full record

ArticleDiabetes2012

Age-related impairment in insulin release: the essential role of β(2)-adrenergic receptor.

Gaetano Santulli, Angela Lombardi, Daniela Sorriento, Antonio Anastasio, Carmine Del Giudice, Pietro Formisano, Francesco Béguinot, Bruno Trimarco, Claudia Miele, Guido Iaccarino

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 pooled it
12.9field-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

63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Central βVeterinary research communications · 2026
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  5. bioRxiv : the preprint server for biology · 2026
    Article
  6. Exploring the mechanisms connecting the sympathetic nervous system and type 2 diabetes: Focus on renal denervation.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2026
    Review
  7. Article
  8. Observational
  9. The mitochondrial enzyme pyruvate carboxylase restricts pancreatic β-cell senescence by blocking p53 activation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Review
  11. Adrenoceptor Expression and Function in the Endocrine Pancreas.Handbook of experimental pharmacology · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

3 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 2 countries.

Gaetano SantulliDepartment of Clinical Medicine, Cardiovascular & Immunologic Sciences, Federico II University of Naples, Naples, Italy.
Angela Lombardi
Daniela Sorriento
Antonio Anastasio
Carmine Del Giudice
Pietro Formisano
Francesco Béguinot
Bruno Trimarco
Claudia Miele
Guido Iaccarino
University of Naples Federico II · ITInstitute for Experimental Endocrinology and Oncology · ITColumbia University Irving Medical Center · USUniversity of Salerno · IT

Funding

Telethon GGP09012
6 · The paper itself

Abstract

In this study, we investigated the significance of β(2)-adrenergic receptor (β(2)AR) in age-related impaired insulin secretion and glucose homeostasis. We characterized the metabolic phenotype of β(2)AR-null C57Bl/6N mice (β(2)AR(-/-)) by performing in vivo and ex vivo experiments. In vitro assays in cultured INS-1E β-cells were carried out in order to clarify the mechanism by which β(2)AR deficiency affects glucose metabolism. Adult β(2)AR(-/-) mice featured glucose intolerance, and pancreatic islets isolated from these animals displayed impaired glucose-induced insulin release, accompanied by reduced expression of peroxisome proliferator-activated receptor (PPAR)γ, pancreatic duodenal homeobox-1 (PDX-1), and GLUT2. Adenovirus-mediated gene transfer of human β(2)AR rescued these defects. Consistent effects were evoked in vitro both upon β(2)AR knockdown and pharmacologic treatment. Interestingly, with aging, wild-type (β(2)AR(+/+)) littermates developed impaired insulin secretion and glucose tolerance. Moreover, islets from 20-month-old β(2)AR(+/+) mice exhibited reduced density of β(2)AR compared with those from younger animals, paralleled by decreased levels of PPARγ, PDX-1, and GLUT2. Overexpression of β(2)AR in aged mice rescued glucose intolerance and insulin release both in vivo and ex vivo, restoring PPARγ/PDX-1/GLUT2 levels. Our data indicate that reduced β(2)AR expression contributes to the age-related decline of glucose tolerance in mice.

Indexed as

Age FactorsAnimalsGlucose Tolerance TestGlucose Transporter Type 2Homeodomain ProteinsInsulinMaleMiceMice, Inbred C57BLPhenotypePPAR gammaReceptors, Adrenergic, beta-2Trans-ActivatorsGlucose Transporter Type 2Homeodomain ProteinsInsulinpancreatic and duodenal homeobox 1 proteinPPAR gammaReceptors, Adrenergic, beta-2Slc2a2 protein, mouseTrans-Activators

Identifiers

PMID22315324
PMCPMC3282797
OpenAlexW2095949680

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.