Evidence map›Paper›PMID 25310607›Full record

ArticlePloS one2014

Laminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain.

Marcella K Vaicik, Jill Thyboll Kortesmaa, Sofia Movérare-Skrtic, Jarkko Kortesmaa, Raija Soininen, Göran Bergström, Claes Ohlsson, Li Yen Chong, Björn Rozell, Margo Emont and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 64 citations in OpenAlex.

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  18. Recent Developments in Extracellular Matrix Remodeling for Fat Grafting.Frontiers in cell and developmental biology · 2021
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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

13 authors at 7 institutions in 3 countries.

Marcella K VaicikDepartment of Biomedical Engineering, Illinois Institute of Technology, Chicago, Illinois, United States of America.
Jill Thyboll KortesmaaDivision of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Sofia Movérare-SkrticCenter for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, Gothenburg University, Göteborg, Sweden.
Jarkko KortesmaaDivision of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Raija SoininenDivision of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Göran BergströmDepartment of Molecular and Clinical Medicine, Sahlgrenska University Hospital, Göteborg, Sweden.
Claes OhlssonCenter for Bone and Arthritis Research, Institute of Medicine, The Sahlgrenska Academy, Gothenburg University, Göteborg, Sweden.
Li Yen ChongCardiovascular and Metabolic Disorders Program, Duke-NUS Graduate Medical School, Singapore, Singapore.
Björn RozellClinical Research Center and Division of Pathology, Infectious Diseases, Department of Immunology, Microbiology, Pathology, and Infectious Diseases, Karolinska Institutet, Huddinge University Hospital, Stockholm, Sweden.
Margo EmontSection of Endocrinology, Department of Medicine, University of Chicago, Chicago, Illinois, United States of America.
Ronald N CohenSection of Endocrinology, Department of Medicine, University of Chicago, Chicago, Illinois, United States of America.
Eric M BreyDepartment of Biomedical Engineering, Illinois Institute of Technology, Chicago, Illinois, United States of America; Research Service, Hines Veteran Affairs Hospital, Hines, Illinois, United States of America.
Karl TryggvasonDivision of Matrix Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden; Cardiovascular and Metabolic Disorders Program, Duke-NUS Graduate Medical School, Singapore, Singapore.
Karolinska Institutet · SEUniversity of Chicago · USUniversity of Gothenburg · SEDuke-NUS Medical School · SGEdward Hines, Jr. VA Hospital · USIllinois Institute of Technology · USSahlgrenska University Hospital · SE

Funding

Pilot and Feasibility ProgramP30DK020595 · NIDDK · UNIVERSITY OF CHICAGO · PI Matthew J Brady · 2013 to 2026
$20.9M
Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
NCATS NIH HHS UL1 TR000430NIDDK NIH HHS P30 DK020595
6 · The paper itself

Abstract

Obesity is a global epidemic that contributes to the increasing medical burdens related to type 2 diabetes, cardiovascular disease and cancer. A better understanding of the mechanisms regulating adipose tissue expansion could lead to therapeutics that eliminate or reduce obesity-associated morbidity and mortality. The extracellular matrix (ECM) has been shown to regulate the development and function of numerous tissues and organs. However, there is little understanding of its function in adipose tissue. In this manuscript we describe the role of laminin α4, a specialized ECM protein surrounding adipocytes, on weight gain and adipose tissue function. Adipose tissue accumulation, lipogenesis, and structure were examined in mice with a null mutation of the laminin α4 gene (Lama4-/-) and compared to wild-type (Lama4+/+) control animals. Lama4-/- mice exhibited reduced weight gain in response to both age and high fat diet. Interestingly, the mice had decreased adipose tissue mass and altered lipogenesis in a depot-specific manner. In particular, epididymal adipose tissue mass was specifically decreased in knock-out mice, and there was also a defect in lipogenesis in this depot as well. In contrast, no such differences were observed in subcutaneous adipose tissue at 14 weeks. The results suggest that laminin α4 influences adipose tissue structure and function in a depot-specific manner. Alterations in laminin composition offers insight into the roll the ECM potentially plays in modulating cellular behavior in adipose tissue expansion.

Indexed as

Weight GainAdipocytesAdipose TissueAdipose Tissue, WhiteAgingAnimalsCell SizeDiet, High-FatFeeding BehaviorLamininLipogenesisMaleMice, Inbred C57BLObesitySubcutaneous FatLama4 protein, mouseLaminin

Identifiers

PMID25310607
PMCPMC4195691
OpenAlexW2063939463

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.