Evidence map›Paper›PMID 22389718›Full record

ArticlePloS one2012

Adipocyte-specific protein tyrosine phosphatase 1B deletion increases lipogenesis, adipocyte cell size and is a minor regulator of glucose homeostasis.

Carl Owen, Alicja Czopek, Abdelali Agouni, Louise Grant, Robert Judson, Emma K Lees, George D Mcilroy, Olga Göransson, Andy Welch, Kendra K Bence and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.5field-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

39 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Review
  3. Endothelial Dysfunction in Obesity and Therapeutic Targets.Advances in experimental medicine and biology · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Journal of clinical medicine · 2021
    Article
  11. Adipocyte GNature communications · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

14 authors at 5 institutions in 4 countries.

Carl OwenIntegrative Physiology, University of Aberdeen, Aberdeen, United Kingdom.
Alicja Czopek
Abdelali Agouni
Louise Grant
Robert Judson
Emma K Lees
George D Mcilroy
Olga Göransson
Andy Welch
Kendra K Bence
Barbara B Kahn
Benjamin G Neel
Nimesh Mody
Mirela Delibegović
University of Aberdeen · GBBeth Israel Deaconess Medical Center · USLund University · SEPrincess Margaret Cancer Centre · CAUniversity of Pennsylvania · US

Funding

Glucose Transporter Regulation in Obesity and DiabetesR37DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 2006 to 2015
$5.0M
British Heart Foundation PG/09/048/27675British Heart Foundation PG/11/8/28703NIDDK NIH HHS R37 DK043051
6 · The paper itself

Abstract

Protein tyrosine phosphatase 1B (PTP1B), a key negative regulator of leptin and insulin signaling, is positively correlated with adiposity and contributes to insulin resistance. Global PTP1B deletion improves diet-induced obesity and glucose homeostasis via enhanced leptin signaling in the brain and increased insulin signaling in liver and muscle. However, the role of PTP1B in adipocytes is unclear, with studies demonstrating beneficial, detrimental or no effect(s) of adipose-PTP1B-deficiency on body mass and insulin resistance. To definitively establish the role of adipocyte-PTP1B in body mass regulation and glucose homeostasis, adipocyte-specific-PTP1B knockout mice (adip-crePTP1B(-/-)) were generated using the adiponectin-promoter to drive Cre-recombinase expression. Chow-fed adip-crePTP1B(-/-) mice display enlarged adipocytes, despite having similar body weight/adiposity and glucose homeostasis compared to controls. High-fat diet (HFD)-fed adip-crePTP1B(-/-) mice display no differences in body weight/adiposity but exhibit larger adipocytes, increased circulating glucose and leptin levels, reduced leptin sensitivity and increased basal lipogenesis compared to controls. This is associated with decreased insulin receptor (IR) and Akt/PKB phosphorylation, increased lipogenic gene expression and increased hypoxia-induced factor-1-alpha (Hif-1α) expression. Adipocyte-specific PTP1B deletion does not beneficially manipulate signaling pathways regulating glucose homeostasis, lipid metabolism or adipokine secretion in adipocytes. Moreover, PTP1B does not appear to be the major negative regulator of the IR in adipocytes.

Indexed as

AdipocytesAnimalsBlotting, WesternBody CompositionCells, CulturedCell SizeGlucoseHomeostasisImmunoprecipitationLipogenesisMiceMice, Mutant StrainsPositron-Emission TomographyProtein Tyrosine Phosphatase, Non-Receptor Type 1GlucoseProtein Tyrosine Phosphatase, Non-Receptor Type 1

Identifiers

PMID22389718
PMCPMC3289674
OpenAlexW2067657272

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.