Evidence map›Paper›PMID 17657604›Full record

ReviewReviews in endocrine & metabolic disorders2007

Metabolic programming in the pathogenesis of insulin resistance.

Sherin U Devaskar, Manikkavasagar Thamotharan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.9field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Observational
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Epigenetic and microRNA-mediated regulation in diabetes.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2009
    Article
  18. The developmental origins of adult disease.Current opinion in pediatrics · 2009
    Review
  19. Dry foods and risk of disease in cats.The Canadian veterinary journal = La revue veterinaire canadienne · 2008
    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

2 authors at 1 institution in 1 country.

Sherin U DevaskarDivision of Neonatology & Developmental Biology and the Neonatal Research Center, Department of Pediatrics, David Geffen School of Medicine UCLA, Los Angeles, CA 90095-1752, USA. sdevaskar@mednet.ucla.edu
Manikkavasagar Thamotharan
University of California, Los Angeles · US

Funding

Prenatal Metabolic Programming of the OffspringR01HD041230 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 2001 to 2019
$5.2M
POSTNATAL ASPECTS OF A GLUCOSE TRANSPORTERR01HD033997 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 1995 to 2008
$3.1M
PERINATAL METABOLIC AND HORMONAL EFFECTSR01HD025024 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 1996 to 2010
$2.6M
Role of Placental Transport In Fetal GrowthR01HD046979 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 2004 to 2008
$1.7M
DEVELOPMENTAL REGULATION OF NEURON INSULIN-LIKE PEPTIDER29HD025024 · NICHD · SAINT LOUIS UNIVERSITY · PI DEVASKAR, SHERIN U. · 1989 to 1993
–
NICHD NIH HHS HD-25024NICHD NIH HHS HD-33997NICHD NIH HHS HD-41230NICHD NIH HHS HD-46979
6 · The paper itself

Abstract

This review focuses on different animal models of nutrient perturbations, inclusive of restrictive and excessive states mimicking human situations during pregnancy and lactation that cause aberrations in the offspring. These aberrations consist of diminished insulin sensitivity in the presence of defective insulin production. These phenotypic changes are due to altered peripheral tissue post-insulin receptor signaling mechanisms and pancreatic beta-islet insulin synthesis and secretion defects. While these changes during in utero or postnatal life serve as essential adaptations to overcome adverse conditions, they become maladaptive subsequently and set the stage for type 2 diabetes mellitus. Pregnancy leads to gestational diabetes with trans-generational propagation of the insulin resistant phenotype. This is in response to the metabolically aberrant maternal in utero environment, and tissue specific epigenetic perturbations that permanently alter expression of critical genes transmitted to future generations. These heritable aberrations consisting of altered DNA methylation and histone modifications remodel chromatin and affect transcription of key genes. Along with an altered in utero environment, these chromatin modifications contribute to the world-wide epidemic of type 2 diabetes mellitus, with nutrient excess dominating in developed and nutrient restriction in developing countries.

Indexed as

AcetylationAnimalsDiabetes Mellitus, Type 2DNA MethylationFemaleHistonesHumansInsulin ResistanceModels, BiologicalPregnancyHistones

Identifiers

PMID17657604
OpenAlexW1997542436

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.