Evidence map›Paper›PMID 19589948›Full record

ReviewEndocrine reviews2009

The role of liver-derived insulin-like growth factor-I.

Claes Ohlsson, Subburaman Mohan, Klara Sjögren, Asa Tivesten, Jörgen Isgaard, Olle Isaksson, John-Olov Jansson, Johan Svensson

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 3 pooled it
18.6field-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

188 citing papers in PubMed, 3 syntheses or guidelines pooled it, 449 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  13. Asparagine endopeptidase prompts breast cancer-related pericardial calcification by regulating IGF2 and integrin αvβ5.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  18. Drug discovery targeting thyroid hormone receptorActa pharmaceutica Sinica. B · 2025
    Review
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128 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

8 authors at 4 institutions in 2 countries.

Claes OhlssonDivision of Endocrinology, Institute of Medicine, Sahlgrenska University Hospital, Göteborg, Sweden. Claes.Ohlsson@medic.gu.se
Subburaman Mohan
Klara Sjögren
Asa Tivesten
Jörgen Isgaard
Olle Isaksson
John-Olov Jansson
Johan Svensson
National Academy of Medicine · USSahlgrenska University Hospital · SEJerry L. Pettis Memorial VA Medical Center · USUniversity of Gothenburg · SE

Funding

Transgenic Approaches to Evaluate IGF-I Role in Peak BMDR01AR048139 · NIAMS · LOMA LINDA VETERANS ASSN RESEARCH &EDUC · PI MOHAN, SUBBURAMAN · 2003 to 2025
$4.7M
ENDOSTEAL BONE VOLUME REGULATION AND OSTEOPOROSISR01AR031062 · NIAMS · LOMA LINDA VETERANS ASSN RESEARCH &EDUC · PI MOHAN, SUBBURAMAN · 1986 to 2014
$3.5M
Transgenic Approaches to Evalute IGF-1 Role in Peak BMDR56AR048139 · NIAMS · LOMA LINDA VETERANS ASSN RESEARCH & EDUC · PI MOHAN, SUBBURAMAN · 2008 to 2008
$258k
NIAMS NIH HHS AR-031062NIAMS NIH HHS AR-048139NIAMS NIH HHS R01 AR031062NIAMS NIH HHS R01 AR048139NIAMS NIH HHS R56 AR048139
6 · The paper itself

Abstract

IGF-I is expressed in virtually every tissue of the body, but with much higher expression in the liver than in any other tissue. Studies using mice with liver-specific IGF-I knockout have demonstrated that liver-derived IGF-I, constituting a major part of circulating IGF-I, is an important endocrine factor involved in a variety of physiological and pathological processes. Detailed studies comparing the impact of liver-derived IGF-I and local bone-derived IGF-I demonstrate that both sources of IGF-I can stimulate longitudinal bone growth. We propose here that liver-derived circulating IGF-I and local bone-derived IGF-I to some extent have overlapping growth-promoting effects and might have the capacity to replace each other (= redundancy) in the maintenance of normal longitudinal bone growth. Importantly, and in contrast to the regulation of longitudinal bone growth, locally derived IGF-I cannot replace (= lack of redundancy) liver-derived IGF-I for the regulation of a large number of other parameters including GH secretion, cortical bone mass, kidney size, prostate size, peripheral vascular resistance, spatial memory, sodium retention, insulin sensitivity, liver size, sexually dimorphic liver functions, and progression of some tumors. It is clear that a major role of liver-derived IGF-I is to regulate GH secretion and that some, but not all, of the phenotypes in the liver-specific IGF-I knockout mice are indirect, mediated via the elevated GH levels. All of the described multiple endocrine effects of liver-derived IGF-I should be considered in the development of possible novel treatment strategies aimed at increasing or reducing endocrine IGF-I activity.

Indexed as

AnimalsBody CompositionBone and BonesBone DevelopmentGrowth HormoneHumansInsulin-Like Growth Factor ILiverGrowth HormoneInsulin-Like Growth Factor I

Identifiers

PMID19589948
PMCPMC2759708
OpenAlexW2127573768

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.