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Interplay of Dietary Fatty Acids and Cholesterol Impacts Brain Mitochondria and Insulin Action

Title data

Schell, Mareike ; Chudoba, Chantal ; Leboucher, Antoine ; Alfine, Eugenia ; Flore, Tanina ; Ritter, Katrin ; Weiper, Katharina ; Wernitz, Andreas ; Henkel, Janin ; Kleinridders, André:
Interplay of Dietary Fatty Acids and Cholesterol Impacts Brain Mitochondria and Insulin Action.
In: Nutrients. Vol. 12 (23 May 2020) Issue 5 .
ISSN 2072-6643
DOI: https://doi.org/10.3390/nu12051518

Abstract in another language

Overconsumption of high-fat and cholesterol-containing diets is detrimental for metabolism and mitochondrial function, causes inflammatory responses and impairs insulin action in peripheral tissues. Dietary fatty acids can enter the brain to mediate the nutritional status, but also to influence neuronal homeostasis. Yet, it is unclear whether cholesterol-containing high-fat diets (HFDs) with different combinations of fatty acids exert metabolic stress and impact mitochondrial function in the brain. To investigate whether cholesterol in combination with different fatty acids impacts neuronal metabolism and mitochondrial function, C57BL/6J mice received different cholesterol-containing diets with either high concentrations of long-chain saturated fatty acids or soybean oil-derived poly-unsaturated fatty acids. In addition, CLU183 neurons were stimulated with combinations of palmitate, linoleic acid and cholesterol to assess their effects on metabolic stress, mitochondrial function and insulin action. The dietary interventions resulted in a molecular signature of metabolic stress in the hypothalamus with decreased expression of occludin and subunits of mitochondrial electron chain complexes, elevated protein carbonylation, as well as c-Jun N-terminal kinase (JNK) activation. Palmitate caused mitochondrial dysfunction, oxidative stress, insulin and insulin-like growth factor-1 (IGF-1) resistance, while cholesterol and linoleic acid did not cause functional alterations. Finally, we defined insulin receptor as a novel negative regulator of metabolically stress-induced JNK activation.

Further data

Item Type: Article in a journal
Refereed: Yes
Keywords: JNK; brain; cholesterol; fatty acids; inflammation; insulin receptor; insulin signaling; mitochondria
Institutions of the University: Faculties > Faculty of Life Sciences: Food, Nutrition and Health
Result of work at the UBT: No
DDC Subjects: 500 Science
500 Science > 570 Life sciences, biology
Date Deposited: 26 Apr 2021 12:46
Last Modified: 26 Apr 2021 12:56
URI: https://eref.uni-bayreuth.de/id/eprint/64444