Authors
Anne Ladwig, Anna Lena Cremer, Johannes Romer, Valentina Zimmermann, Claus Brandt, Stefan Blaschke, Claudia Orschel, Charlotte Orschel, Marvin Schäfer, Maria A Rueger, Klarissa H Stürner, Gereon R Fink, Michael Schroeter, Heiko Backes
Published in
Brain research. Pages 150623. Nov 06, 2026. Epub Nov 06, 2026.
Abstract
We investigated how an active lifestyle can compensate for poor nutrition. Male mice were either housed in an enriched environment (EE) or under control conditions and received either a high-fat diet (HFD) or a normal chow diet. EE markedly attenuated HFD-induced weight gain and prevented gain of fat mass. However, mice on HFD developed glucose intolerance and insulin resistance regardless of housing conditions. Already one day after onset of the intervention, EE and HFD modulated glucose uptake in feeding-related brain regions. Chronic HFD evoked a considerable reduction of brain glucose metabolism and induced meta-inflammation in the brain, which both were ameliorated by the EE. Following EE withdrawal, HFD-fed mice exhibited rapid weight gain and an elevated ratio of energy intake to expenditure. HFD was associated with increased DeltaFosB expression in the nucleus accumbens and dorsal striatum, brain regions related to reward-driven control of feeding. Our data show that an active lifestyle can only partially compensate for HFD-induced deficits in brain metabolism and inflammation and causes possible detrimental effects to the energy balance after cessation of the activity/exercise paradigm.
PMID:
42994773
Bibliographic data and abstract were imported from PubMed on 07 Nov 2026.
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