Evidence map›Paper›PMID 31061470›Full record

ArticleScientific reports2019

Chronic dysfunction of Stromal interaction molecule by pulsed RNAi induction in fat tissue impairs organismal energy homeostasis in Drosophila.

Yanjun Xu, Annika F Borcherding, Christoph Heier, Gu Tian, Thomas Roeder, Ronald P Kühnlein

Abstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Lipid Metabolism in Relation to Calcium Homeostasis.Advances in experimental medicine and biology · 2026
    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

6 authors.

Yanjun XuMax-Planck-Institut für biophysikalische Chemie, Research Group Molecular Physiology, Am Faβberg 11, D-37077, Göttingen, Germany. yanjun.xu@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0003-3487-717X
Annika F BorcherdingMax-Planck-Institut für biophysikalische Chemie, Research Group Molecular Physiology, Am Faβberg 11, D-37077, Göttingen, Germany.
Christoph HeierUniversity of Graz, Institute of Molecular Biosciences, Humboldtstrasse 50/2.OG, A-8010, Graz, Austria.
Gu TianChristian-Albrechts University Kiel, Zoology, Molecular Physiology, 24098, Kiel, Germany.
Thomas RoederChristian-Albrechts University Kiel, Zoology, Molecular Physiology, 24098, Kiel, Germany.
Ronald P KühnleinMax-Planck-Institut für biophysikalische Chemie, Research Group Molecular Physiology, Am Faβberg 11, D-37077, Göttingen, Germany. ronald.kuehnlein@uni-graz.at.ORCID http://orcid.org/0000-0003-1448-4117

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Drosophila Transgenic RNAi Resource ProjectR01GM084947 · NIGMS · HARVARD MEDICAL SCHOOL · PI PERRIMON, NORBERT · 2008 to 2019
$9.8M
NIGMS NIH HHS R01 GM084947NIH HHS P40 OD018537
6 · The paper itself

Abstract

Obesity is a progressive, chronic disease, which can be caused by long-term miscommunication between organs. It remains challenging to understand how chronic dysfunction in a particular tissue remotely impairs other organs to eventually imbalance organismal energy homeostasis. Here we introduce RNAi Pulse Induction (RiPI) mediated by short hairpin RNA (shRiPI) or double-stranded RNA (dsRiPI) to generate chronic, organ-specific gene knockdown in the adult Drosophila fat tissue. We show that organ-restricted RiPI targeting Stromal interaction molecule (Stim), an essential factor of store-operated calcium entry (SOCE), results in progressive fat accumulation in fly adipose tissue. Chronic SOCE-dependent adipose tissue dysfunction manifests in considerable changes of the fat cell transcriptome profile, and in resistance to the glucagon-like Adipokinetic hormone (Akh) signaling. Remotely, the adipose tissue dysfunction promotes hyperphagia likely via increased secretion of Akh from the neuroendocrine system. Collectively, our study presents a novel in vivo paradigm in the fly, which is widely applicable to model and functionally analyze inter-organ communication processes in chronic diseases.

Indexed as

Adipose TissueAnimalsAspartate Aminotransferase, CytoplasmicCalciumCalcium-Binding ProteinsCalcium SignalingDisease Models, AnimalDrosophila melanogasterDrosophila ProteinsEnergy MetabolismFemaleGene Expression RegulationHomeostasisHumansHyperphagiaInsect HormonesAralar protein, DrosophilaAspartate Aminotransferase, CytoplasmicCalciumCalcium-Binding ProteinsDAKH peptideDrosophila ProteinsInsect HormonesIsoenzymesMalate DehydrogenaseOligopeptidesPyrrolidonecarboxylic AcidRNA, Small InterferingStim protein, DrosophilaStromal Interaction Molecule 1

Identifiers

PMID31061470
PMCPMC6502815

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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.