Evidence map›Paper›PMID 25695774›Full record

ArticlePloS one2015

Defective differentiation of adipose precursor cells from lipodystrophic mice lacking perilipin 1.

Ying Lyu, Xueying Su, Jingna Deng, Shangxin Liu, Liangqiang Zou, Xiaojing Zhao, Suning Wei, Bin Geng, Guoheng Xu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Ying LyuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Xueying SuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Jingna DengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Shangxin LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Liangqiang ZouDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Xiaojing ZhaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Suning WeiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Bin GengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Guoheng XuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Perilipin 1 (Plin1) localizes at the surface of lipid droplets to regulate triglyceride storage and hydrolysis in adipocytes. Plin1 defect leads to low adiposity in mice and partial lipodystrophy in human. This study investigated the roles of Plin1 in adipocyte differentiation. Plin1 null (-/-) mice showed plenty of multilocular adipocytes and small unilocular adipocytes in adipose tissue, along with lack of a subpopulation of adipose progenitor cells capable of in vivo adipogenesis and along with downregulation of adipogenic pathway. Before initiation of differentiation, adipose stromal-vascular cells (SVCs) from Plin1-/- mice already accumulated numerous tiny lipid droplets, which increased in number and size during the first 12-h induction but thereafter became disappeared at day 1 of differentiation. The adipogenic signaling was dysregulated despite protein level of PPARγ was near normal in Plin1-/- SVCs like in Plin1-/- adipose tissue. Heterozygous Plin1+/- SVCs were able to develop lipid droplets, with both the number and size more than in Plin1-/- SVCs but less than in Plin1+/+ SVCs, indicating that Plin1 haploinsufficiency accounts for attenuated adipogenesis. Aberrant lipid droplet growth and differentiation of Plin1-/- SVCs were rescued by adenoviral Plin1 expression and were ameliorated by enhanced or prolonged adipogenic stimulation. Our finding suggests that Plin1 plays an important role in adipocyte differentiation and provides an insight into the pathology of partial lipodystrophy in patients with Plin1 mutation.

Indexed as

1-Methyl-3-isobutylxanthineAdipogenesisAdipose TissueAnimalsCarrier ProteinsCCAAT-Enhancer-Binding ProteinsLipid MetabolismLipodystrophyLipolysisMiceMice, KnockoutMicroscopy, FluorescencePerilipin-1Phosphodiesterase InhibitorsPhosphoproteinsPPAR gamma1-Methyl-3-isobutylxanthineCarrier ProteinsCCAAT-Enhancer-Binding ProteinsPerilipin-1Phosphodiesterase InhibitorsPhosphoproteinsPLIN1 protein, humanPlin1 protein, mousePPAR gammaSrebf1 protein, mouseSterol Regulatory Element Binding Protein 1

Identifiers

PMID25695774
PMCPMC4335001
OpenAlexW1984150591

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.