Evidence map›Paper›PMID 37437545›Full record

ArticleCell metabolism2023

Fetal manipulation of maternal metabolism is a critical function of the imprinted Igf2 gene.

Jorge Lopez-Tello, Hannah E J Yong, Ionel Sandovici, Georgina K C Dowsett, Efthimia R Christoforou, Esteban Salazar-Petres, Rebecca Boyland, Tina Napso, Giles S H Yeo, Brian Y H Lam and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Cell metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
22.5field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 6 institutions in 2 countries.

Jorge Lopez-TelloCentre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK. Electronic address: jl898@cam.ac.uk.
Hannah E J YongCentre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK; Singapore Institute for Clinical Sciences (SICS), Agency for Science, Technology and Research (A(∗)STAR), 30 Medical Drive, Singapore 117609, Singapore.
Ionel SandoviciCentre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK; Department of Obstetrics and Gynaecology and National Institute for Health Research Cambridge Biomedical Research Centre, Cambridge CB2 0SW, UK; Medical Research Council (MRC) Metabolic Diseases Unit, Wellcome-MRC Institute of Metabolic Science and, University of Cambridge, Cambridge CB2 0QQ, UK.
Georgina K C DowsettMedical Research Council (MRC) Metabolic Diseases Unit, Wellcome-MRC Institute of Metabolic Science and, University of Cambridge, Cambridge CB2 0QQ, UK.
Efthimia R ChristoforouCentre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
Esteban Salazar-PetresCentre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
Rebecca BoylandCentre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK; Royal Devon and Exeter Hospital NHS Trust, Barrack Rd, Exeter EX2 5DW, UK.
Tina NapsoCentre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK.
Giles S H YeoMedical Research Council (MRC) Metabolic Diseases Unit, Wellcome-MRC Institute of Metabolic Science and, University of Cambridge, Cambridge CB2 0QQ, UK.
Brian Y H LamMedical Research Council (MRC) Metabolic Diseases Unit, Wellcome-MRC Institute of Metabolic Science and, University of Cambridge, Cambridge CB2 0QQ, UK.
Miguel ConstanciaCentre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK; Department of Obstetrics and Gynaecology and National Institute for Health Research Cambridge Biomedical Research Centre, Cambridge CB2 0SW, UK; Medical Research Council (MRC) Metabolic Diseases Unit, Wellcome-MRC Institute of Metabolic Science and, University of Cambridge, Cambridge CB2 0QQ, UK. Electronic address: jmasmc2@cam.ac.uk.
Amanda N Sferruzzi-PerriCentre for Trophoblast Research, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3EG, UK. Electronic address: ans48@cam.ac.uk.
University of Cambridge · GBMedical Research Council · GBAgency for Science, Technology and Research · SGNIHR Cambridge Biomedical Research CentreRoyal Devon and Exeter Hospital · GBWellcome/MRC Institute of Metabolic Science · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H003312/1British Heart Foundation RG/17/12/33167Cancer Research UKMedical Research Council MC_UU_00014/1Medical Research Council MC_UU_00014/4Medical Research Council MC_UU_00014/5Medical Research Council MC_UU_12012/4Medical Research Council MC_UU_12012/5Medical Research Council MRC_MC_UU_12012/4Medical Research Council MRC_MC_UU_12012/5Medical Research Council MR/R022690/1Medical Research Council MR/R022690/1/RG93186Wellcome TrustWellcome Trust 208363/Z/17/ZWellcome Trust 220456/Z/20/Z
6 · The paper itself

Abstract

Maternal-offspring interactions in mammals involve both cooperation and conflict. The fetus has evolved ways to manipulate maternal physiology to enhance placental nutrient transfer, but the mechanisms involved remain unclear. The imprinted Igf2 gene is highly expressed in murine placental endocrine cells. Here, we show that Igf2 deletion in these cells impairs placental endocrine signaling to the mother, without affecting placental morphology. Igf2 controls placental hormone production, including prolactins, and is crucial to establish pregnancy-related insulin resistance and to partition nutrients to the fetus. Consequently, fetuses lacking placental endocrine Igf2 are growth restricted and hypoglycemic. Mechanistically, Igf2 controls protein synthesis and cellular energy homeostasis, actions dependent on the placental endocrine cell type. Igf2 loss also has additional long-lasting effects on offspring metabolism in adulthood. Our study provides compelling evidence for an intrinsic fetal manipulation system operating in placenta that modifies maternal metabolism and fetal resource allocation, with long-term consequences for offspring metabolic health.

Indexed as

Insulin-Like Growth Factor IIInsulin ResistancePlacentaAnimalsCell CommunicationFemaleGenomic ImprintingHomeostasisHypoglycemic AgentsMicePregnancyHypoglycemic AgentsIGF2 protein, mouseInsulin-Like Growth Factor IIfetal programminggenomic imprintingglucosehormonesinsulin-like growth factor 2metabolismplacentapregnancyprolactin

Identifiers

PMID37437545
PMCPMC7619417
OpenAlexW4383888123

What Socratic 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 Socratic graph.