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@ARTICLE{Tsunekawa:147339,
author = {T. Tsunekawa and R. Banno and H. Yaginuma and K. Taki and
A. Mizoguchi and M. Sugiyama and T. Onoue and H. Takagi and
D. Hagiwara$^*$ and Y. Ito and S. Iwama and M. Goto and H.
Suga and B. Bettler and H. Arima},
title = {{GABAB} {R}eceptor {S}ignaling in the {M}esolimbic {S}ystem
{S}uppresses {B}inge-like {C}onsumption of a {H}igh-{F}at
{D}iet.},
journal = {iScience},
volume = {20},
issn = {2589-0042},
address = {St. Louis},
publisher = {Elsevier},
reportid = {DKFZ-2019-02460},
pages = {337 - 347},
year = {2019},
abstract = {Binge eating could contribute to the development of
obesity, and previous studies suggest
that gamma-aminobutyric acid (GABA) type B receptor
(GABABR) signaling is involved in the regulation of binge
eating. Here, we show that time-restricted access to a
high-fat diet (HFD) induces binge-like eating behavior in
wild-type mice. HFD consumption during restricted time was
significantly increased in corticostriatal neuron-specific
GABABR-deficient mice compared with wild-type mice.
Furthermore, the GABABR agonist baclofen suppressed HFD
intake during restricted time in wild-type mice but not in
corticostriatal or dopaminergic neuron-specific
GABABR-deficient mice. In contrast, there were no
significant differences in food consumption among genotypes
under ad libitum access to HFD. Thus, our data show that the
mesolimbic system regulates food consumption under
time-restricted but not ad libitum access to HFD and have
identified a mechanism by which GABABR signaling suppresses
binge-like eating of HFD.},
cin = {V078},
ddc = {050},
cid = {I:(DE-He78)V078-20160331},
pnm = {319H - Addenda (POF3-319H)},
pid = {G:(DE-HGF)POF3-319H},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31610370},
doi = {10.1016/j.isci.2019.09.032},
url = {https://inrepo02.dkfz.de/record/147339},
}