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  Dietary-challenged mice with Alzheimer-like pathology show increased energy expenditure and reduced adipocyte hypertrophy and steatosis

Schreyer, S., Berndt, N., Eckstein, J., Mülleder, M., Hemmati-Sadeghi, S., Klein, C., et al. (2021). Dietary-challenged mice with Alzheimer-like pathology show increased energy expenditure and reduced adipocyte hypertrophy and steatosis. Aging, 2021: 202978. doi:10.18632/aging.202978.

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© 2021 Schreyer et al

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Schreyer, Stefanie , Author
Berndt, Nikolaus , Author
Eckstein, Johannes , Author
Mülleder, Michael, Author
Hemmati-Sadeghi, Shabnam , Author
Klein, Charlotte, Author
Abuelnor, Basim , Author
Panzel, Alina, Author
Meierhofer, David1, Author              
Spranger, Joachim , Author
Steiner, Barbara, Author
Brachs, Sebastian , Author
Affiliations:
1Mass Spectrometry (Head: David Meierhofer), Scientific Service (Head: Christoph Krukenkamp), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479669              

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 Abstract: Alzheimer’s disease (AD) is frequently accompanied by progressing weight loss, correlating with mortality. Counter-intuitively, weight loss in old age might predict AD onset but obesity in midlife increases AD risk. Furthermore, AD is associated with diabetes-like alterations in glucose metabolism. Here, we investigated metabolic features of amyloid precursor protein overexpressing APP23 female mice modeling AD upon long-term challenge with high-sucrose (HSD) or high-fat diet (HFD). Compared to wild type littermates (WT), APP23 females were less prone to mild HSD-induced and considerable HFD-induced glucose tolerance deterioration, despite unaltered glucose tolerance during normal-control diet. Indirect calorimetry revealed increased energy expenditure and hyperactivity in APP23 females. Dietary interventions, especially HFD, had weaker effects on lean and fat mass gain, steatosis and adipocyte hypertrophy of APP23 than WT mice, as shown by 1H-magnetic-resonance-spectroscopy, histological and biochemical analyses. Proteome analysis revealed differentially regulated expression of mitochondrial proteins in APP23 livers and brains. In conclusion, hyperactivity, increased metabolic rate, and global mitochondrial dysfunction potentially add up to the development of AD-related body weight changes in APP23 females, becoming especially evident during diet-induced metabolic challenge. These findings emphasize the importance of translating this metabolic phenotyping into human research to decode the metabolic component in AD pathogenesis.

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Language(s): eng - English
 Dates: 2021-03-272021-04-16
 Publication Status: Published online
 Pages: -
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 Table of Contents: -
 Rev. Type: -
 Identifiers: DOI: 10.18632/aging.202978
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Title: Aging
  Abbreviation : Aging (Albany NY)
Source Genre: Journal
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Publ. Info: New York : Impact Journals LLC
Pages: - Volume / Issue: 2021 Sequence Number: 202978 Start / End Page: - Identifier: Other: 1945-4589
Other: http://www.sherpa.ac.uk/romeo/issn/1945-4589/
CoNE: https://pure.mpg.de/cone/journals/resource/1945-4589