Evidence map›Paper›PMID 20211984›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2010

Targeted deletion of somatotroph insulin-like growth factor-I signaling in a cell-specific knockout mouse model.

Christopher J Romero, Yewade Ng, Raul M Luque, Rhonda D Kineman, Linda Koch, Jens C Bruning, Sally Radovick

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
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  12. Important Hormones Regulating Lipid Metabolism.Molecules (Basel, Switzerland) · 2022
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  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. DLK1/PREF1 regulates nutrient metabolism and protects from steatosis.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
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

7 authors at 5 institutions in 3 countries.

Christopher J RomeroDivision of Pediatric Endocrinology, Johns Hopkins University School of Medicine, Children's Medical and Surgical Center 4-106, 600 North Wolfe Street, Baltimore, Maryland 21208, USA. cromero5@jhmi.edu
Yewade Ng
Raul M Luque
Rhonda D Kineman
Linda Koch
Jens C Bruning
Sally Radovick
Johns Hopkins University · USUniversity Hospital Cologne · DEUniversity of Cologne · DEUniversity of Córdoba · ESUniversity of Illinois Chicago · US

Funding

Interdepartmental Training Program in Cellular and Molecular EndocrinologyT32DK007751 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WOLFE, ANDREW M · 1997 to 2016
$4.6M
Mouse model of adult-onset, isolated, GH-deficiencyR21AG031465 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI KINEMAN, RHONDA D · 2008 to 2009
$284k
Physiologic Role of the Somatotroph IGF-1 ReceptorF32DK081280 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI ROMERO, CHRISTOPHER JOSEPH · 2008 to 2009
$118k
NIA NIH HHS 5621AG031465VANIA NIH HHS R21 AG031465NIDDK NIH HHS 1F32DK081280-01NIDDK NIH HHS F32 DK081280NIDDK NIH HHS T32 DK007751NIDDK NIH HHS T32DK07751
6 · The paper itself

Abstract

The role of IGF-I in the negative regulation of GH expression and release is demonstrated by in vitro and in vivo models; however, the targets and mechanisms of IGF-I remain unclear. We have developed a cell-specific knockout mouse in which the IGF-I receptor was ablated from the somatotroph in order to validate and characterize IGF-I negative regulation; we termed this the somatotroph IGF-I receptor knockout (SIGFRKO) mouse. The SIGFRKO mice demonstrated increased GH gene expression and secretion as well as increased serum IGF-I. Compensatory changes were noted with decreased GHRH and increased somatostatin mRNA expression levels. SIGFRKO mice had normal linear growth, but by 14 wk of age weighed significantly less than controls. Furthermore, metabolic studies revealed SIGFRKO mice had significantly less fat mass and body percent fat. These data support somatotroph IGF-I negative regulation and suggest that hypothalamic feedback limits the extent of GH release. The SIGFRKO mouse is a model delineating the mechanisms of IGF-I regulation in the hypothalamic-pituitary axis and demonstrates compensatory mechanisms that mediate growth and metabolic function in mammals.

Indexed as

Adipose TissueAnimalsBlotting, WesternFemaleGrowth HormoneGrowth Hormone-Releasing HormoneInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IMagnetic Resonance ImagingMaleMiceMice, KnockoutModels, AnimalOrgan SizeReceptor, IGF Type 1Receptors, NeuropeptideGrowth HormoneGrowth Hormone-Releasing HormoneInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor IReceptor, IGF Type 1Receptors, NeuropeptideReceptors, Pituitary Hormone-Regulating HormoneSomatostatinsomatotropin releasing hormone receptor

Identifiers

PMID20211984
PMCPMC2870932
OpenAlexW1974228571

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.