Evidence map›Paper›PMID 22923471›Full record

ArticleDiabetes2012

A new role for lipocalin prostaglandin d synthase in the regulation of brown adipose tissue substrate utilization.

Sam Virtue, Helena Feldmann, Mark Christian, Chong Yew Tan, Mojgan Masoodi, Martin Dale, Chris Lelliott, Keith Burling, Mark Campbell, Naomi Eguchi and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-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

24 citing papers in PubMed, 50 citations in OpenAlex.

  1. Lipocalin-type prostaglandin D synthase scavenges biliverdin in the cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014
    Trial
  2. Article
  3. Review
  4. Lipocalin-Type Prostaglandin DPharmaceutical research · 2022
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Inflammatory Signaling and Brown Fat Activity.Frontiers in endocrinology · 2020
    Review
  12. Article
  13. Review
  14. L-PGDS-produced PGDScientific reports · 2019
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. The brain and brown fat.Annals of medicine · 2015
    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

17 authors at 3 institutions in 2 countries.

Sam VirtueUniversity of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke’s Treatment Centre, Addenbrooke’s Hospital, Cambridge, U.K. sv234@medschl.cam.ac.uk
Helena Feldmann
Mark Christian
Chong Yew Tan
Mojgan Masoodi
Martin Dale
Chris Lelliott
Keith Burling
Mark Campbell
Naomi Eguchi
Peter Voshol
Jaswinder K Sethi
Malcolm Parker
Yoshihiro Urade
Julian L Griffin
Barbara Cannon
Antonio Vidal-Puig
Osaka Science Museum · JPWenner-Gren Foundations · SEAstraZeneca (Sweden) · SE

Funding

Biotechnology and Biological Sciences Research Council BB/H013539/1Biotechnology and Biological Sciences Research Council JF16994British Heart Foundation PG/10/38/28359Medical Research Council G0600717Medical Research Council G0802051Medical Research Council MC_UP_A090_1006
6 · The paper itself

Abstract

In this study, we define a new role for lipocalin prostaglandin D synthase (L-PGDS) in the control of metabolic fuel utilization by brown adipose tissue (BAT). We demonstrate that L-PGDS expression in BAT is positively correlated with BAT activity, upregulated by peroxisome proliferator-activated receptor γ coactivator 1α or 1β and repressed by receptor-interacting protein 140. Under cold-acclimated conditions, mice lacking L-PGDS had elevated reliance on carbohydrate to provide fuel for thermogenesis and had increased expression of genes regulating glycolysis and de novo lipogenesis in BAT. These transcriptional differences were associated with increased lipid content in BAT and a BAT lipid composition enriched with de novo synthesized lipids. Consistent with the concept that lack of L-PGDS increases glucose utilization, mice lacking L-PGDS had improved glucose tolerance after high-fat feeding. The improved glucose tolerance appeared to be independent of changes in insulin sensitivity, as insulin levels during the glucose tolerance test and insulin, leptin, and adiponectin levels were unchanged. Moreover, L-PGDS knockout mice exhibited increased expression of genes involved in thermogenesis and increased norepinephrine-stimulated glucose uptake to BAT, suggesting that sympathetically mediated changes in glucose uptake may have improved glucose tolerance. Taken together, these results suggest that L-PGDS plays an important role in the regulation of glucose utilization in vivo.

Indexed as

Adipose Tissue, BrownAnimalsBody CompositionCell LineFemaleIntramolecular OxidoreductasesLipocalinsMaleMiceReal-Time Polymerase Chain ReactionThermogenesisTriglyceridesIntramolecular OxidoreductasesLipocalinsprostaglandin R2 D-isomeraseTriglycerides

Identifiers

PMID22923471
PMCPMC3501861
OpenAlexW2114881431

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.