Evidence map›Paper›PMID 24748928›Full record

ReviewWorld journal of diabetes2014

Knockout mouse models of insulin signaling: Relevance past and future.

Anne E Bunner, P Charukeshi Chandrasekera, Neal D Barnard

Abstract readReview
In one paragraph

Review in World journal of diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Review
  7. Article
  8. Glucose Metabolism in Burns-What Happens?International journal of molecular sciences · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Sex Differences in Androgen Regulation of Metabolism in Nonhuman Primates.Advances in experimental medicine and biology · 2017
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
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

3 authors.

Anne E BunnerAnne E Bunner, P Charukeshi Chandrasekera, Neal D Barnard, Physicians Committee for Responsible Medicine, Washington, DC 20016, United States.
P Charukeshi ChandrasekeraAnne E Bunner, P Charukeshi Chandrasekera, Neal D Barnard, Physicians Committee for Responsible Medicine, Washington, DC 20016, United States.
Neal D BarnardAnne E Bunner, P Charukeshi Chandrasekera, Neal D Barnard, Physicians Committee for Responsible Medicine, Washington, DC 20016, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance is a hallmark of type 2 diabetes. In an effort to understand and treat this condition, researchers have used genetic manipulation of mice to uncover insulin signaling pathways and determine the effects of their perturbation. After decades of research, much has been learned, but the pathophysiology of insulin resistance in human diabetes remains controversial, and treating insulin resistance remains a challenge. This review will discuss limitations of mouse models lacking select insulin signaling molecule genes. In the most influential mouse models, glucose metabolism differs from that of humans at the cellular, organ, and whole-organism levels, and these differences limit the relevance and benefit of the mouse models both in terms of mechanistic investigations and therapeutic development. These differences are due partly to immutable differences in mouse and human biology, and partly to the failure of genetic modifications to produce an accurate model of human diabetes. Several factors often limit the mechanistic insights gained from experimental mice to the particular species and strain, including: developmental effects, unexpected metabolic adjustments, genetic background effects, and technical issues. We conclude that the limitations and weaknesses of genetically modified mouse models of insulin resistance underscore the need for redirection of research efforts toward methods that are more directly relevant to human physiology.

Indexed as

Disease models, AnimalGlucose/metabolismInsulin resistanceKnockoutMiceSignal transduction

Identifiers

PMID24748928
PMCPMC3990311

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.