Evidence map›Paper›PMID 23589828›Full record

ReviewPhysiological reviews2013

Somatotropic signaling: trade-offs between growth, reproductive development, and longevity.

Andrzej Bartke, Liou Y Sun, Valter Longo

Abstract readReview
In one paragraph

Review in Physiological reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 1 pooled it
8.8field-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

166 citing papers in PubMed, 1 synthesis or guideline pooled it, 283 citations in OpenAlex.

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  19. Nutrition, GH/IGF-1 signaling, and cancer.Endocrine-related cancer · 2024
    Review
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106 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

3 authors at 2 institutions in 1 country.

Andrzej BartkeSouthern Illinois University School of Medicine, Department of Internal Medicine, Geriatric Research, Springfield, Illinois 62703, USA. abartke@siumed.edu
Liou Y Sun
Valter Longo
University of Southern California · USMichigan Medicine · US

Funding

The Role of the Glucose-regulated Protein GRP78/BiP in Stress Resistance and AginP01AG034906 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LONGO, VALTER D. · 2011 to 2016
$9.3M
The Somatotropic Axis and Health Aging: A Search for MechanismsP01AG031736 · NIA · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI KIRKLAND, JAMES L. · 2009 to 2013
$8.4M
Longevity genes and calorie restriction: early post-natal effectsR01AG019899 · NIA · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI BARTKE, ANDRZEJ · 2001 to 2016
$6.1M
Role of Longevity Regulatory Pathways in Age-dependent Macro-molecular Damage inR01AG020642 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LONGO, VALTER D. · 2003 to 2017
$4.8M
Chronological Age-Dependent Genomic Instability in YeastR01AG025135 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LONGO, VALTER D. · 2006 to 2010
$1.3M
Developmental Origins of Phenotypic Characteristics that Predict LongevityR21AG038850 · NIA · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI BARTKE, ANDRZEJ · 2011 to 2012
$328k
NIA NIH HHS AG025135NIA NIH HHS AG20642NIA NIH HHS P01 AG031736NIA NIH HHS P01 AG034906NIA NIH HHS R01 AG019899NIA NIH HHS R01 AG020642NIA NIH HHS R21 AG038850
6 · The paper itself

Abstract

Growth hormone (GH) is a key determinant of postnatal growth and plays an important role in the control of metabolism and body composition. Surprisingly, deficiency in GH signaling delays aging and remarkably extends longevity in laboratory mice. In GH-deficient and GH-resistant animals, the "healthspan" is also extended with delays in cognitive decline and in the onset of age-related disease. The role of hormones homologous to insulin-like growth factor (IGF, an important mediator of GH actions) in the control of aging and lifespan is evolutionarily conserved from worms to mammals with some homologies extending to unicellular yeast. The combination of reduced GH, IGF-I, and insulin signaling likely contributes to extended longevity in GH or GH receptor-deficient organisms. Diminutive body size and reduced fecundity of GH-deficient and GH-resistant mice can be viewed as trade-offs for extended longevity. Mechanisms responsible for delayed aging of GH-related mutants include enhanced stress resistance and xenobiotic metabolism, reduced inflammation, improved insulin signaling, and various metabolic adjustments. Pathological excess of GH reduces life expectancy in men as well as in mice, and GH resistance or deficiency provides protection from major age-related diseases, including diabetes and cancer, in both species. However, there is yet no evidence of increased longevity in GH-resistant or GH-deficient humans, possibly due to non-age-related deaths. Results obtained in GH-related mutant mice provide striking examples of mutations of a single gene delaying aging, reducing age-related disease, and extending lifespan in a mammal and providing novel experimental systems for the study of mechanisms of aging.

Indexed as

Signal TransductionAnimalsGrowth HormoneHumansLongevityReceptors, SomatotropinReproductionGrowth HormoneReceptors, Somatotropin

Identifiers

PMID23589828
PMCPMC3768106
OpenAlexW2125246804

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.