Evidence map›Paper›PMID 20974668›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

Lipocalin 2 is a selective modulator of peroxisome proliferator-activated receptor-gamma activation and function in lipid homeostasis and energy expenditure.

Daozhong Jin, Hong Guo, So Young Bu, Yuanyuan Zhang, Jennifer Hannaford, Douglas G Mashek, Xiaoli Chen

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 85 citations in OpenAlex.

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  13. Plasma Lipocalin-2 and Adiponectin are Affected by Obesity Rather Than Type 2 Diabetes Mellitus per se.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
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  20. Lipocalin-2 abrogates epithelial cell cycle arrest by PPARγ inhibition.Laboratory investigation; a journal of technical methods and pathology · 2018
    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

7 authors at 3 institutions in 1 country.

Daozhong JinDepartment of Food Science and Nutrition, University of Minnesota-Twin Cities, St. Paul, MN 55108-1038, USA.
Hong Guo
So Young Bu
Yuanyuan Zhang
Jennifer Hannaford
Douglas G Mashek
Xiaoli Chen
Twin Cities Orthopedics · USTwin Cities Public Television · USUniversity of Minnesota · US

Funding

Lipocalin 2 in Inflammation and Metabolic ControlR01DK080743 · NIDDK · UNIVERSITY OF MINNESOTA · PI CHEN, XIAOLI · 2008 to 2012
$1.5M
NIDDK NIH HHS R01 DK080743NIDDK NIH HHS R01DK080743
6 · The paper itself

Abstract

We have previously identified lipocalin 2 (Lcn2) as a cytokine playing a critical role in the regulation of body fat mass, lipid metabolism, and insulin resistance. Lcn2 deficiency reduces PPARγ gene expression in adipocytes. In this study, we investigated the role of Lcn2 in PPARγ activation and function via assessing the insulin sensitization and fatty acid (FA) homeostasis of PPARγ agonist in high-fat diet (HFD)-induced obesity in Lcn2(-/-) mice. We found that rosiglitazone (Rosi) significantly improved insulin sensitivity in Lcn2(-/-) mice as effectively as in wild-type (WT) mice; unfed-state levels of blood glucose, free FAs, and triglycerides (TGs) were significantly reduced after a 25-d treatment of Rosi in Lcn2(-/-) mice. However, Rosi action on fat deposition and FA homeostasis was altered; Rosi-induced body weight and subcutaneous fat gain and liver lipid accumulation were markedly lessened in Lcn2(-/-) mice. The results of in vivo metabolic labeling showed that Rosi markedly reduced de novo lipogenesis in adipose tissue of Lcn2(-/-) mice. In brown adipose tissue (BAT), the expression of the genes functioning in TG hydrolysis and mitochondrial oxidation was up-regulated more in Lcn2(-/-) than in WT mice. Most strikingly, Rosi stimulated significantly higher levels of uncoupling protein-1 expression in BAT, and completely rescued cold intolerance in Lcn2(-/-) mice. We demonstrate that Lcn2 is a critical selective modulator of PPARγ activation and function in lipid homeostasis and energy expenditure.

Indexed as

Acute-Phase ProteinsAdipocytesAdipose Tissue, BrownAnimalsDietary FatsEnergy MetabolismHomeostasisHypoglycemic AgentsLipid MetabolismLipocalin-2LipocalinsMiceMice, Inbred C57BLMice, KnockoutObesityOncogene Proteins2,4-thiazolidinedioneAcute-Phase ProteinsDietary FatsHypoglycemic AgentsLcn2 protein, mouseLipocalin-2LipocalinsOncogene ProteinsPPAR gammaRosiglitazoneThiazolidinediones

Identifiers

PMID20974668
PMCPMC3023388
OpenAlexW2018630214

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.