Evidence map›Paper›PMID 27511834›Full record

ArticleScientific reports2016

Transgenic overexpression of VEGF-C induces weight gain and insulin resistance in mice.

Sinem Karaman, Maija Hollmén, Sun-Young Yoon, H Furkan Alkan, Kari Alitalo, Christian Wolfrum, Michael Detmar

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.0field-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

36 citing papers in PubMed, 49 citations in OpenAlex.

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  14. The Role of VEGF Family in Lipid Metabolism.Current pharmaceutical biotechnology · 2023
    Article
  15. Lymphatics in Cardiovascular Physiology.Cold Spring Harbor perspectives in medicine · 2022
    Review
  16. Lymphangiogenesis and Lymphatic Barrier Dysfunction in Renal Fibrosis.International journal of molecular sciences · 2022
    Review
  17. Review
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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

7 authors at 3 institutions in 2 countries.

Sinem KaramanInstitute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland.
Maija HollménInstitute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland.
Sun-Young YoonInstitute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland.
H Furkan AlkanInstitute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland.
Kari AlitaloWihuri Research Institute and Translational Cancer Biology Program, Biomedicum Helsinki, University of Helsinki, Finland.
Christian WolfrumInstitute of Food, Nutrition and Health, Swiss Federal Institute of Technology, ETH Zurich, 8603 Schwerzenbach, Switzerland.
Michael DetmarInstitute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, 8093 Zurich, Switzerland.
ETH Zurich · CHÉcole Polytechnique Fédérale de Lausanne · CHUniversity of Helsinki · FI

Funding

Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

Obesity comprises great risks for human health, contributing to the development of other diseases such as metabolic syndrome, type 2 diabetes and cardiovascular disease. Previously, obese patients were found to have elevated serum levels of VEGF-C, which correlated with worsening of lipid parameters. We recently identified that neutralization of VEGF-C and -D in the subcutaneous adipose tissue during the development of obesity improves metabolic parameters and insulin sensitivity in mice. To test the hypothesis that VEGF-C plays a role in the promotion of the metabolic disease, we used K14-VEGF-C mice that overexpress human VEGF-C under control of the keratin-14 promoter in the skin and monitored metabolic parameters over time. K14-VEGF-C mice had high levels of VEGF-C in the subcutaneous adipose tissue and gained more weight than wildtype littermates, became insulin resistant and had increased ectopic lipid accumulation at 20 weeks of age on regular mouse chow. The metabolic differences persisted under high-fat diet induced obesity. These results indicate that elevated VEGF-C levels contribute to metabolic deterioration and the development of insulin resistance, and that blockade of VEGF-C in obesity represents a suitable approach to alleviate the development of insulin resistance.

Indexed as

Gene Expression RegulationInsulin ResistancePromoter Regions, GeneticAnimalsHumansKeratin-14MaleMiceMice, TransgenicObesityOrgan SpecificitySubcutaneous FatVascular Endothelial Growth Factor CKeratin-14Krt14 protein, mouseVascular Endothelial Growth Factor CVEGFC protein, human

Identifiers

PMID27511834
PMCPMC4980670
OpenAlexW2514690814

What OpenQuestion holds

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LicenceCC BY
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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.