Evidence map›Paper›PMID 25244225›Full record

ArticleAging cell2014

Specific suppression of insulin sensitivity in growth hormone receptor gene-disrupted (GHR-KO) mice attenuates phenotypic features of slow aging.

Oge Arum, Ravneet K Boparai, Jamal K Saleh, Feiya Wang, Angela L Dirks, Jeremy G Turner, John J Kopchick, Jun-Li Liu, Romesh K Khardori, Andrzej Bartke

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Association between caffeine intake and fat free mass index: a retrospective cohort study.Journal of the International Society of Sports Nutrition · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
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  9. Review
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  11. Article
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  13. Article
  14. Article
  15. Review
  16. Article
  17. Enhanced Cognition and Hypoglutamatergic Signaling in a Growth Hormone Receptor Knockout Mouse Model of Successful Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017
    Article
  18. Obesity and related consequences to ageing.Age (Dordrecht, Netherlands) · 2016
    Review
  19. Article
  20. The somatotropic axis and longevity in mice.American journal of physiology. Endocrinology and metabolism · 2015
    Review
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.

Oge ArumDepartment of Internal Medicine, Southern Illinois University-School of Medicine, Springfield, IL, 62794, USA.
Ravneet K Boparai
Jamal K Saleh
Feiya Wang
Angela L Dirks
Jeremy G Turner
John J Kopchick
Jun-Li Liu
Romesh K Khardori
Andrzej Bartke
Southern Illinois University School of Medicine · USEastern Virginia Medical School · USMcGill University Health Centre · CAOhio University · US

Funding

Systems BiologyU19AG023122 · NIA · TRANSLATIONAL GENOMICS RESEARCH INST · PI NICHOLAS Joseph SCHORK · 2004 to 2026
$102.6M
Longevity genes and calorie restriction: early post-natal effectsR01AG019899 · NIA · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI BARTKE, ANDRZEJ · 2001 to 2016
$6.1M
NIA NIH HHS 3R01AG019899-07S1NIA NIH HHS AG19899NIA NIH HHS R01 AG019899NIA NIH HHS U19 AG023122
6 · The paper itself

Abstract

In addition to their extended lifespans, slow-aging growth hormone receptor/binding protein gene-disrupted (knockout) (GHR-KO) mice are hypoinsulinemic and highly sensitive to the action of insulin. It has been proposed that this insulin sensitivity is important for their longevity and increased healthspan. We tested whether this insulin sensitivity of the GHR-KO mouse is necessary for its retarded aging by abrogating that sensitivity with a transgenic alteration that improves development and secretory function of pancreatic β-cells by expressing Igf-1 under the rat insulin promoter 1 (RIP::IGF-1). The RIP::IGF-1 transgene increased circulating insulin content in GHR-KO mice, and thusly fully normalized their insulin sensitivity, without affecting the proliferation of any non-β-cell cell types. Multiple (nonsurvivorship) longevity-associated physiological and endocrinological characteristics of these mice (namely beneficial blood glucose regulatory control, altered metabolism, and preservation of memory capabilities) were partially or completely normalized, thus supporting the causal role of insulin sensitivity for the decelerated senescence of GHR-KO mice. We conclude that a delayed onset and/or decreased pace of aging can be hormonally regulated.

Indexed as

AgingAnimalsFemaleInsulinInsulin-Like Growth Factor IInsulin ResistanceLongevityMaleMiceMice, KnockoutPhenotypeReceptors, SomatotropinInsulinInsulin-Like Growth Factor IReceptors, Somatotropinendocrinology and metabolismgrowth hormone hormonal signalinginsulin sensitivitylongevity regulation(neuro)endocrinology of senescence

Identifiers

PMID25244225
PMCPMC4326932
OpenAlexW2078282576

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.