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- W2799486570 abstract "Mitochondria are fundamental for cellular metabolism and take center stage in the regulation of systemic energy metabolism. They are origin and target of nutrient intermediates of converging metabolic pathways. Thus, it is essential to maintain mitochondrial homoeostasis. Cells harbor a large set of mitochondrial proteases involved in quality control, including the ATP-dependent Clp protease (CLPP). However, CLPP not only degrades misfolded or damaged proteins, CLPP is also involved in highly regulated proteolytic activities. Many bacterial and mammalian ClpXP substrates have been identified in various metabolic pathways. This study analyzes the role of CLPP in mammalian metabolism using whole body and tissue-specific Clpp knockout mouse models.The ubiquitous loss of CLPP under normal dietary conditions leads to a lean phenotype with enhanced glucose metabolism. The absence of CLPP further facilitates increased energy expenditure in part by WAT browning, despite decreased physical activity. Moreover, CLPP was shown to be involved in fatty acid oxidation by the regulation of its putative substrate VLCAD. In addition, CLPP has a critical role in BAT homeostasis and cold induced thermogenesis. The mild to moderate mitochondrial dysfunction caused by the loss of CLPP in various tissues, induced the expression of the mitokine FGF21. However, using Clpp/Fgf21 double knockout mice, it could be shown that FGF21 is not mediating the metabolic changes observed in CLPP deficient mice.The tissue-specific depletion of CLPP in liver or skeletal muscle and heart revealed a dispensable role for CLPP with regard to whole body metabolism, although tissue restricted mitochondrial dysfunction was present. Finally, ablation of CLPP was demonstrated to protect against HFD induced obesity and insulin resistance. Remarkably, HFD-feeding impaired hepatic mitochondrial translation in the absence of CLPP resulting in decreased complex subunits and decreased supercomplexes levels in an alternate mechanism as previously described for the heart. Thus, mitochondrial CLPP has a critical role in metabolic stress conditions in particular during cold exposure and high fat diet feeding. Therefore, by analyzing CLPP protease function and its link to metabolic stress this study may help to understand pathologies with deregulated Clpp expression." @default.
- W2799486570 created "2018-05-17" @default.
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- W2799486570 date "2017-01-01" @default.
- W2799486570 modified "2023-09-23" @default.
- W2799486570 title "Role of the mitochondrial ATP-dependent Clp protease in mammalian metabolism" @default.
- W2799486570 hasPublicationYear "2017" @default.
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