Evidence map›Paper›PMID 12588883›Full record

ArticleThe Journal of clinical investigation2003

Inhibition of adipogenesis and development of glucose intolerance by soluble preadipocyte factor-1 (Pref-1).

Kichoon Lee, Josep A Villena, Yang Soo Moon, Kee-Hong Kim, Sunjoo Lee, Chulho Kang, Hei Sook Sul

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

112 citing papers in PubMed, 257 citations in OpenAlex.

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  18. Functional Identification of PorcineAnimals : an open access journal from MDPI · 2022
    Article
  19. Review
  20. Retinol Binding Protein 7 Promotes AdipogenesisFrontiers in cell and developmental biology · 2022
    Article

52 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

7 authors at 1 institution in 1 country.

Kichoon LeeDepartment of Nutritional Sciences and Toxicology, and. Cancer Research Laboratory, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720, USA.
Josep A Villena
Yang Soo Moon
Kee-Hong Kim
Sunjoo Lee
Chulho Kang
Hei Sook Sul
University of California, Berkeley · US

Funding

REGULATION OF PREF-1 GENE IN ADIPOCYTE DIFFERENTIATIONR01DK050828 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI SUL, HEI SOOK · 1995 to 2013
$3.5M
NIDDK NIH HHS DK-20828NIDDK NIH HHS R01 DK050828
6 · The paper itself

Abstract

Preadipocyte factor-1 (Pref-1) is a transmembrane protein highly expressed in preadipocytes. Pref-1 expression is, however, completely abolished in adipocytes. The extracellular domain of Pref-1 undergoes two proteolytic cleavage events that generate 50 and 25 kDa soluble products. To understand the function of Pref-1, we generated transgenic mice that express the full ectodomain corresponding to the large cleavage product of Pref-1 fused to human immunoglobulin-gamma constant region. Mice expressing the Pref-1/hFc transgene in adipose tissue, driven by the adipocyte fatty acid-binding protein (aP2, also known as aFABP) promoter, showed a substantial decrease in total fat pad weight. Moreover, adipose tissue from transgenic mice showed reduced expression of adipocyte markers and adipocyte-secreted factors, including leptin and adiponectin, whereas the preadipocyte marker Pref-1 was increased. Pref-1 transgenic mice with a substantial, but not complete, loss of adipose tissue exhibited hypertriglyceridemia, impaired glucose tolerance, and decreased insulin sensitivity. Mice expressing the Pref-1/hFc transgene exclusively in liver under the control of the albumin promoter also showed a decrease in adipose mass and adipocyte marker expression, suggesting an endocrine mode of action of Pref-1. These findings demonstrate the inhibition of adipogenesis by Pref-1 in vivo and the resulting impairment of adipocyte function that leads to the development of metabolic abnormalities.

Indexed as

AdipocytesAnimalsBase SequenceBone and BonesCalcium-Binding ProteinsCell CountCell DifferentiationCell SizeDNA, ComplementaryFemaleGene ExpressionGlucose IntoleranceGrowth DisordersHumansImmunoglobulin Fc FragmentsIntercellular Signaling Peptides and ProteinsCalcium-Binding ProteinsDLK1 protein, humanDlk1 protein, mouseDNA, ComplementaryImmunoglobulin Fc FragmentsIntercellular Signaling Peptides and ProteinsMembrane ProteinsRecombinant Fusion ProteinsRepressor Proteins

Identifiers

PMID12588883
PMCPMC151920
OpenAlexW2115630287

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.