Evidence map›Paper›PMID 15143198›Full record

ArticleMolecular and cellular biology2004

Increased insulin sensitivity and reduced adiposity in phosphatidylinositol 5-phosphate 4-kinase beta-/- mice.

Katja A Lamia, Odile D Peroni, Young-Bum Kim, Lucia E Rameh, Barbara B Kahn, Lewis C Cantley

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

67 citing papers in PubMed, 122 citations in OpenAlex.

  1. PIP4K attenuates PIP5K lipid kinase activity by disrupting membrane-mediated dimerization.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  12. Development of potent and selective degraders of PI5P4Kγ.European journal of medicinal chemistry · 2023
    Article
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  14. Article
  15. Review
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  17. Article
  18. When PIPFrontiers in cell and developmental biology · 2022
    Review
  19. Review
  20. Article

7 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

6 authors at 2 institutions in 2 countries.

Katja A LamiaBeth Israel Hospital, Harvard Institutes of Medicine, Division of Signal Transduction, 10th Floor, 330 Brookline, MA 02215, USA.
Odile D Peroni
Young-Bum Kim
Lucia E Rameh
Barbara B Kahn
Lewis C Cantley
Hadassah Medical Center · ILBoston Biomedical Research Institute · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
Transgenic CoreP30DK057521 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI FLOREZ, JOSE CARLOS · 2000 to 2019
$31.4M
Glucose Transporter Regulation in Obesity and DiabetesR37DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 2006 to 2015
$5.0M
GLUCOSE TRANSPORTER REGULATION IN OBESITY AND DIABETESR01DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 1992 to 2020
$4.4M
The Role of PI3K in Growth RegulationR01GM041890 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI CANTLEY, LEWIS C. · 1990 to 2016
$4.1M
PHOSPHATIDYLINOSITOL KINASESR01GM036624 · NIGMS · TUFTS UNIVERSITY BOSTON · PI CANTLEY, LEWIS C. · 1986 to 2008
$2.9M
Protein Tyrosine Phosphatase 1B and Insulin ActionR01DK060839 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B · 2002 to 2005
$1.7M
Glucose Transporter Regulation in Obesity and DiabetesR56DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 2022 to 2022
$173k
NIDDK NIH HHS 5 P30 DK36836-15NIDDK NIH HHS DK43051NIDDK NIH HHS DK57521NIDDK NIH HHS DK60839NIDDK NIH HHS P30 DK036836NIDDK NIH HHS P30 DK057521NIDDK NIH HHS R01 DK043051NIDDK NIH HHS R01 DK060839NIDDK NIH HHS R37 DK043051NIDDK NIH HHS R56 DK043051NIGMS NIH HHS GM36624NIGMS NIH HHS R01 GM036624NIGMS NIH HHS R01 GM041890
6 · The paper itself

Abstract

Phosphorylated derivatives of the lipid phosphatidylinositol are known to play critical roles in insulin response. Phosphatidylinositol 5-phosphate 4-kinases convert phosphatidylinositol 5-phosphate to phosphatidylinositol 4,5-bis-phosphate. To understand the physiological role of these kinases, we generated mice that do not express phosphatidylinositol 5-phosphate 4-kinase beta. These mice are hypersensitive to insulin and have reduced body weights compared to wild-type littermates. While adult male mice lacking phosphatidylinositol 5-phosphate 4-kinase beta have significantly less body fat than wild-type littermates, female mice lacking phosphatidylinositol 5-phosphate 4-kinase beta have increased insulin sensitivity in the presence of normal adiposity. Furthermore, in vivo insulin-induced activation of the protein kinase Akt is enhanced in skeletal muscle and liver from mice lacking phosphatidylinositol 5-phosphate 4-kinase beta. These results indicate that phosphatidylinositol 5-phosphate 4-kinase beta plays a role in determining insulin sensitivity and adiposity in vivo and suggest that inhibitors of this enzyme may be useful in the treatment of type 2 diabetes.

Indexed as

Adipose TissueAnimalsEatingFemaleInsulinLeptinMaleMiceMice, KnockoutMuscle, SkeletalPhosphatidylinositol PhosphatesPhosphotransferasesInsulinLeptinphosphatidylinositol 5-phosphatePhosphatidylinositol PhosphatesPhosphotransferases

Identifiers

PMID15143198
PMCPMC416424
OpenAlexW2120166232

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.