Chronic dysfunction of Stromal interaction molecule by pulsed RNAi induction in fat tissue impairs organismal energy homeostasis in Drosophila.
Adipose Tissue
/ metabolism
Animals
Aspartate Aminotransferase, Cytoplasmic
/ genetics
Calcium
/ metabolism
Calcium Signaling
Calcium-Binding Proteins
/ genetics
Disease Models, Animal
Drosophila Proteins
/ antagonists & inhibitors
Drosophila melanogaster
Energy Metabolism
/ genetics
Female
Gene Expression Regulation
Homeostasis
/ genetics
Humans
Hyperphagia
/ genetics
Insect Hormones
/ genetics
Ion Transport
Isoenzymes
/ genetics
Lipid Metabolism
/ genetics
Malate Dehydrogenase
/ genetics
Male
Obesity
/ genetics
Oligopeptides
/ genetics
Pyrrolidonecarboxylic Acid
/ analogs & derivatives
RNA, Small Interfering
/ genetics
Stromal Interaction Molecule 1
/ antagonists & inhibitors
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
06 05 2019
06 05 2019
Historique:
received:
10
07
2018
accepted:
15
04
2019
entrez:
8
5
2019
pubmed:
8
5
2019
medline:
15
9
2020
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 31061470
doi: 10.1038/s41598-019-43327-y
pii: 10.1038/s41598-019-43327-y
pmc: PMC6502815
doi:
Substances chimiques
Aralar protein, Drosophila
0
Calcium-Binding Proteins
0
Drosophila Proteins
0
Insect Hormones
0
Isoenzymes
0
Oligopeptides
0
RNA, Small Interfering
0
Stim protein, Drosophila
0
Stromal Interaction Molecule 1
0
DAKH peptide
129204-82-6
Malate Dehydrogenase
EC 1.1.1.37
Aspartate Aminotransferase, Cytoplasmic
EC 2.6.1.-
Calcium
SY7Q814VUP
Pyrrolidonecarboxylic Acid
SZB83O1W42
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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