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Müller, Luisa; Power Guerra, Nicole; Schildt, Anna; Lindner, Tobias; Stenzel, Jan; Behrangi, Newshan; Bergner, Carina; Alberts, Teresa; Bühler, Daniel; Kurth, Jens; Krause, Bernd Joachim; Janowitz, Deborah; Teipel, Stefan; Vollmar, Brigitte; Kuhla, Angela

[18F]GE-180-PET and Post Mortem Marker Characteristics of Long-Term High-Fat-Diet-Induced Chronic Neuroinflammation in Mice

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  • Media type: E-Article
  • Title: [18F]GE-180-PET and Post Mortem Marker Characteristics of Long-Term High-Fat-Diet-Induced Chronic Neuroinflammation in Mice
  • Contributor: Müller, Luisa; Power Guerra, Nicole; Schildt, Anna; Lindner, Tobias; Stenzel, Jan; Behrangi, Newshan; Bergner, Carina; Alberts, Teresa; Bühler, Daniel; Kurth, Jens; Krause, Bernd Joachim; Janowitz, Deborah; Teipel, Stefan; Vollmar, Brigitte; Kuhla, Angela
  • Published: MDPI AG, 2023
  • Published in: Biomolecules, 13 (2023) 5, Seite 769
  • Language: English
  • DOI: 10.3390/biom13050769
  • ISSN: 2218-273X
  • Keywords: Molecular Biology ; Biochemistry
  • Origination:
  • Footnote:
  • Description: <jats:p>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.</jats:p>
  • Access State: Open Access