Evidence map›Paper›PMID 17562854›Full record

ArticleMolecular and cellular biology2007

Mice with a disruption of the imprinted Grb10 gene exhibit altered body composition, glucose homeostasis, and insulin signaling during postnatal life.

Florentia M Smith, Lowenna J Holt, Alastair S Garfield, Marika Charalambous, Francoise Koumanov, Mark Perry, Reto Bazzani, Steven A Sheardown, Bronwyn D Hegarty, Ruth J Lyons and 3 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The insulin signalling network.Nature metabolism · 2025
    Review
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  16. Article
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  18. Article
  19. Genomic imprinting and its effects on postnatal growth and adult metabolism.Cellular and molecular life sciences : CMLS · 2019
    Review
  20. Article

11 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

13 authors at 5 institutions in 2 countries.

Florentia M SmithUniversity of Bath, Developmental Biology Program and Centre for Regenerative Medicine, Department of Biology and Biochemistry, Claverton Down, Bath BA2 7AY, United Kingdom.
Lowenna J Holt
Alastair S Garfield
Marika Charalambous
Francoise Koumanov
Mark Perry
Reto Bazzani
Steven A Sheardown
Bronwyn D Hegarty
Ruth J Lyons
Gregory J Cooney
Roger J Daly
Andrew Ward
University of Bath · GBGarvan Institute of Medical Research · AUSt Vincent's Hospital Sydney · AUGlaxoSmithKline (United Kingdom) · GBUniversity of Bristol · GB

Funding

Medical Research Council G0300415
6 · The paper itself

Abstract

The Grb10 adapter protein is capable of interacting with a variety of receptor tyrosine kinases, including, notably, the insulin receptor. Biochemical and cell culture experiments have indicated that Grb10 might act as an inhibitor of insulin signaling. We have used mice with a disruption of the Grb10 gene (Grb10Delta2-4 mice) to assess whether Grb10 might influence insulin signaling and glucose homeostasis in vivo. Adult Grb10Delta2-4 mice were found to have improved whole-body glucose tolerance and insulin sensitivity, as well as increased muscle mass and reduced adiposity. Tissue-specific changes in insulin receptor tyrosine phosphorylation were consistent with a model in which Grb10, like the closely related Grb14 adapter protein, prevents specific protein tyrosine phosphatases from accessing phosphorylated tyrosines within the kinase activation loop. Furthermore, insulin-induced IRS-1 tyrosine phosphorylation was enhanced in Grb10Delta2-4 mutant animals, supporting a role for Grb10 in attenuation of signal transmission from the insulin receptor to IRS-1. We have previously shown that Grb10 strongly influences growth of the fetus and placenta. Thus, Grb10 forms a link between fetal growth and glucose-regulated metabolism in postnatal life and is a candidate for involvement in the process of fetal programming of adult metabolic health.

Indexed as

Body CompositionHomeostasisAdipose Tissue, WhiteAdiposityAnimalsAnimals, NewbornBody WeightEnzyme ActivationFeeding BehaviorGenomic ImprintingGlucoseGRB10 Adaptor ProteinInsulinLeptinMaleMiceGlucoseGRB10 Adaptor ProteinInsulinLeptinPhosphotyrosineProto-Oncogene Proteins c-aktReceptor, IGF Type 1Receptor, Insulin

Identifiers

PMID17562854
PMCPMC1952119
OpenAlexW2093517093

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.