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@ARTICLE{Mller:258254,
author = {Müller, Luisa and Power Guerra, Nicole and Schildt, Anna
and Lindner, Tobias and Stenzel, Jan and Behrangi, Newshan
and Bergner, Carina and Alberts, Teresa and Bühler, Daniel
and Kurth, Jens and Krause, Bernd Joachim and Janowitz,
Deborah and Teipel, Stefan and Vollmar, Brigitte and Kuhla,
Angela},
title = {[18{F}]{GE}-180-{PET} and {P}ost {M}ortem {M}arker
{C}haracteristics of {L}ong-{T}erm
{H}igh-{F}at-{D}iet-{I}nduced {C}hronic {N}euroinflammation
in {M}ice.},
journal = {Biomolecules},
volume = {13},
number = {5},
issn = {2218-273X},
address = {Basel},
publisher = {MDPI},
reportid = {DZNE-2023-00600},
pages = {769},
year = {2023},
abstract = {Obesity is characterized by immoderate fat accumulation
leading to an elevated risk of neurodegenerative disorders,
along with a host of metabolic disturbances. Chronic
neuroinflammation is a main factor linking obesity and the
propensity for neurodegenerative disorders. To determine the
cerebrometabolic effects of diet-induced obesity (DIO) in
female mice fed a long-term (24 weeks) high-fat diet (HFD,
$60\%$ fat) compared to a group on a control diet (CD,
$20\%$ fat), we used in vivo PET imaging with the
radiotracer [18F]FDG as a marker for brain glucose
metabolism. In addition, we determined the effects of DIO on
cerebral neuroinflammation using translocator protein 18 kDa
(TSPO)-sensitive PET imaging with [18F]GE-180. Finally, we
performed complementary post mortem histological and
biochemical analyses of TSPO and further microglial (Iba1,
TMEM119) and astroglial (GFAP) markers as well as cerebral
expression analyses of cytokines (e.g., Interleukin
(IL)-1β). We showed the development of a peripheral DIO
phenotype, characterized by increased body weight, visceral
fat, free triglycerides and leptin in plasma, as well as
increased fasted blood glucose levels. Furthermore, we found
obesity-associated hypermetabolic changes in brain glucose
metabolism in the HFD group. Our main findings with respect
to neuroinflammation were that neither [18F]GE-180 PET nor
histological analyses of brain samples seem fit to detect
the predicted cerebral inflammation response, despite clear
evidence of perturbed brain metabolism along with elevated
IL-1β expression. These results could be interpreted as a
metabolically activated state in brain-resident immune cells
due to a long-term HFD.},
keywords = {Mice / Female / Animals / Diet, High-Fat: adverse effects /
Neuroinflammatory Diseases / Obesity: diagnostic imaging /
Obesity: metabolism / Carrier Proteins / Neurodegenerative
Diseases / Glucose / Positron-Emission Tomography: methods /
Mice, Inbred C57BL / TSPO (Other) / [18F]FDG PET/CT (Other)
/ [18F]GE-180 PET/CT (Other) / diet-induced obesity (Other)
/ high-fat diet (Other) / neuroinflammation (Other) / GE-180
(NLM Chemicals) / Carrier Proteins (NLM Chemicals) / Glucose
(NLM Chemicals)},
cin = {AG Teipel},
ddc = {570},
cid = {I:(DE-2719)1510100},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37238638},
pmc = {pmc:PMC10216137},
doi = {10.3390/biom13050769},
url = {https://pub.dzne.de/record/258254},
}