Evidence map›Paper›PMID 10501653›Full record

ReviewMolecular medicine (Cambridge, Mass.)1999

Diabetes and the role of inositol-containing lipids in insulin signaling.

D R Jones, I Varela-Nieto

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular medicine (Cambridge, Mass.), 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  9. Article
  10. Inositols in Insulin Signaling and Glucose Metabolism.International journal of endocrinology · 2018
    Review
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  13. Review
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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.

D R JonesDepartment of Immunology and Oncology, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas, Cantoblanco, Madrid, Spain. djones@cnb.uam.es
I Varela-Nieto
Consejo Superior de Investigaciones Científicas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among metabolic diseases, diabetes is considered one of the most prevalent throughout the world. Currently, statistics show that over 10% of the world's aged population (60 years and older) suffers from diabetes. As a consequence, it consumes a considerable proportion of world health expenditure. This review considers both past and current research into the molecular basis of insulin resistance found in type II diabetes and focuses on the role of inositol-containing phospholipid metabolism. It has been firmly established that the activation of phosphatidylinositol 3-kinase (PI3-K) is important for the propagation of the metabolic actions of insulin. In addition to the 3-phosphorylated phosphatidylinositols formed via the action of PI3-K, the glycosyl-phosphatidylinositol/inositol phosphoglycan (GPI/IPG) signaling component is also strongly implicated in mediating numerous metabolic actions of insulin. Although all the elements within the type II diabetes phenotype have not been fully defined, it has been proposed that defects in insulin transmembrane signaling through malfunction of inositol-containing phospholipid metabolism and absenteeism of the generation of phospholipid-derived second messengers may be associated with the appearance of the type II diabetic phenotype. Pharmaceutical approaches using synthetically produced IPG analogues, which themselves mimic insulin's actions, alone or in combination with other drugs, may lead the way toward introducing alternative therapies for type II diabetes in the coming years.

Indexed as

Signal TransductionAgedAnimalsDiabetes Mellitus, Type 2HumansInsulinInsulin ResistanceMiddle AgedPhosphatidylinositol 3-KinasesPhosphatidylinositolsPrevalenceInsulinPhosphatidylinositol 3-KinasesPhosphatidylinositols

Identifiers

PMID10501653
PMCPMC2230454
OpenAlexW1270603611

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.