Evidence map›Paper›PMID 19497975›Full record

ArticleEndocrinology2009

Elevated levels of insulin-like growth factor (IGF)-I in serum rescue the severe growth retardation of IGF-I null mice.

Yingjie Wu, Hui Sun, Shoshana Yakar, Derek LeRoith

Abstract read
In one paragraph

Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
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

47 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Identification andFrontiers in endocrinology · 2021
    Article
  17. Article
  18. Review
  19. IGF-1 and cardiovascular disease.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2019
    Review
  20. 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

4 authors.

Yingjie WuDivision of Endocrinology, Diabetes, and Bone Disease, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.
Hui Sun
Shoshana Yakar
Derek LeRoith

Funding

Mechanisms for the pro-metastatic effects of hyperinsulinemia on breast cancerR01CA128799 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEROITH, DEREK · 2008 to 2018
$3.7M
SERUM IGF-1 DELIVERY SYSTEM AND ITS ROLE IN DETERMINING SKELETAL INTEGRITYR01AR054919 · NIAMS · NEW YORK UNIVERSITY · PI YAKAR, SHOSHANA · 2007 to 2011
$1.8M
THE TEMPORAL AND SPATIAL REGULATION OF BONE ACQUISITION BY SERUM IGF-1R01AR055141 · NIAMS · NEW YORK UNIVERSITY · PI YAKAR, SHOSHANA · 2008 to 2012
$1.8M
NCI NIH HHS 1R01CA128799NCI NIH HHS R01 CA128799NIAMS NIH HHS AR054919NIAMS NIH HHS AR055141NIAMS NIH HHS R01 AR054919NIAMS NIH HHS R01 AR055141
6 · The paper itself

Abstract

IGF-I plays a vital role in growth and development and acts in an endocrine and an autocrine/paracrine fashion. The purpose of the current study was to clarify whether elevated levels of IGF-I in serum can rescue the severe growth retardation and organ development and function of igf-I null mice. To address that, we overexpressed a rat igf-I transgene specifically in the liver of igf-I null mice. We found that in the total absence of tissue IGF-I, elevated levels of IGF-I in serum can support normal body size at puberty and after puberty but are insufficient to fully support the female reproductive system (evident by irregular estrous cycle, impaired development of ovarian corpus luteum, reduced number of uterine glands and endometrial hypoplasia, all leading to decreased number of pregnancies and litter size). We conclude that most autocrine/paracrine actions of IGF-I that determine organ growth and function can be compensated by elevated levels of endocrine IGF-I. However, in mice, full compensatory responses are evident later in development, suggesting that autocrine/paracrine IGF-I is critical for neonatal development. Furthermore, we show that tissue IGF-I is necessary for the development of the female reproductive system and cannot be compensated by elevated levels of serum IGF-I.

Indexed as

AnimalsEstrous CycleFemaleGene Expression Regulation, DevelopmentalGrowthGrowth HormoneInsulinInsulin-Like Growth Factor IMiceMice, KnockoutMice, TransgenicRatsReproductionGrowth HormoneInsulinInsulin-Like Growth Factor I

Identifiers

PMID19497975
PMCPMC2819739

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.