% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Manire:138795,
author = {Manière, Gérard and Ziegler, Anna B and Geillon, Flore
and Featherstone, David E and Grosjean, Yael},
title = {{D}irect {S}ensing of {N}utrients via a {LAT}1-like
{T}ransporter in {D}rosophila {I}nsulin-{P}roducing
{C}ells.},
journal = {Cell reports},
volume = {17},
number = {1},
issn = {2211-1247},
address = {[New York, NY]},
publisher = {Elsevier},
reportid = {DZNE-2020-05117},
pages = {137-148},
year = {2016},
abstract = {Dietary leucine has been suspected to play an important
role in insulin release, a hormone that controls satiety and
metabolism. The mechanism by which insulin-producing cells
(IPCs) sense leucine and regulate insulin secretion is still
poorly understood. In Drosophila, insulin-like peptides
(DILP2 and DILP5) are produced by brain IPCs and are
released in the hemolymph after leucine ingestion. Using
Ca(2+)-imaging and ex vivo cultured larval brains, we
demonstrate that IPCs can directly sense extracellular
leucine levels via minidiscs (MND), a leucine transporter.
MND knockdown in IPCs abolished leucine-dependent changes,
including loss of DILP2 and DILP5 in IPC bodies, consistent
with the idea that MND is necessary for leucine-dependent
DILP release. This, in turn, leads to a strong increase in
hemolymph sugar levels and reduced growth. GDH knockdown in
IPCs also reduced leucine-dependent DILP release, suggesting
that nutrient sensing is coupled to the glutamate
dehydrogenase pathway.},
keywords = {Amino Acid Transport Systems: genetics / Amino Acid
Transport Systems: metabolism / Animals / Brain: cytology /
Brain: metabolism / Calcium: metabolism / Drosophila
Proteins: genetics / Drosophila Proteins: metabolism /
Drosophila melanogaster: cytology / Drosophila melanogaster:
metabolism / Gene Expression Regulation / Glutamate
Dehydrogenase: genetics / Glutamate Dehydrogenase:
metabolism / Hemolymph: metabolism / Insulin-Secreting
Cells: cytology / Insulin-Secreting Cells: metabolism /
Insulins: genetics / Insulins: metabolism / Larva: cytology
/ Larva: metabolism / Leucine: administration $\&$ dosage /
Leucine: metabolism / Protein Isoforms: genetics / Protein
Isoforms: metabolism / Signal Transduction / Amino Acid
Transport Systems (NLM Chemicals) / Drosophila Proteins (NLM
Chemicals) / Ilp5 protein, Drosophila (NLM Chemicals) /
Insulins (NLM Chemicals) / Mnd protein, Drosophila (NLM
Chemicals) / Protein Isoforms (NLM Chemicals) / Glutamate
Dehydrogenase (NLM Chemicals) / Leucine (NLM Chemicals) /
Calcium (NLM Chemicals)},
cin = {AG Tavosanis},
ddc = {610},
cid = {I:(DE-2719)1013018},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:27681427},
pmc = {pmc:PMC5055474},
doi = {10.1016/j.celrep.2016.08.093},
url = {https://pub.dzne.de/record/138795},
}