Evidence map›Paper›PMID 21537430›Full record

ArticleWorld journal of diabetes2010

Molecular mechanisms of insulin resistance in type 2 diabetes mellitus.

Vandana Saini

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in World journal of diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
5.8field-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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 282 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Synthesis and structure-activity relationship studies of 1,2,4-triazole-benzoxazepine hybrids as α-glucosidase inhibitors: molecular docking and biological evaluation.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Article
  7. Review
  8. Bacterial pyruvate metabolism regulates host insulin sensitivity inbioRxiv : the preprint server for biology · 2026
    Article
  9. Review
  10. Review
  11. Article
  12. The role of PYY in improving insulin resistance.Frontiers in endocrinology · 2026
    Review
  13. Article
  14. Expanding the understanding of insulin resistance in brain and periphery.Trends in endocrinology and metabolism: TEM · 2026
    Review
  15. Review
  16. Review
  17. Article
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  19. Review
  20. Review

41 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

1 author at 1 institution in 1 country.

Vandana SainiVandana Saini, Department of Biochemistry, Lady Hardinge Medical College, New Delhi 110001, India.
Lady Hardinge Medical College · IN

Funding

LIVER REGENERATION IN PEDIATRIC LIVER DISEASEK08DK002900 · NIDDK · WASHINGTON UNIVERSITY · PI RUDNICK, DAVID A · 2000 to 2004
$546k
NIDDK NIH HHS K08 DK002900
6 · The paper itself

Abstract

Free fatty acids are known to play a key role in promoting loss of insulin sensitivity in type 2 diabetes mellitus but the underlying mechanism is still unclear. It has been postulated that an increase in the intracellular concentration of fatty acid metabolites activates a serine kinase cascade, which leads to defects in insulin signaling downstream to the insulin receptor. In addition, the complex network of adipokines released from adipose tissue modulates the response of tissues to insulin. Among the many molecules involved in the intracellular processing of the signal provided by insulin, the insulin receptor substrate-2, the protein kinase B and the forkhead transcription factor Foxo 1a are of particular interest, as recent data has provided strong evidence that dysfunction of these proteins results in insulin resistance in vivo. Recently, studies have revealed that phosphoinositidedependent kinase 1-independent phosphorylation of protein kinase Cε causes a reduction in insulin receptor gene expression. Additionally, it has been suggested that mitochondrial dysfunction triggers activation of several serine kinases, and weakens insulin signal transduction. Thus, in this review, the current developments in understanding the pathophysiological processes of insulin resistance in type 2 diabetes have been summarized. In addition, this study provides potential new targets for the treatment and prevention of type 2 diabetes.

Indexed as

AdipokinesForkhead box protein OInsulin receptorInsulin receptor substrate proteinsInsulin resistanceInsulin signalingPhosphatidylinositol 3-kinaseProtein kinase BType 2 diabetes mellitus

Identifiers

PMID21537430
PMCPMC3083885
OpenAlexW2021010709

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.