mTORC1 controls fasting-induced ketogenesis and its modulation by ageing

By Shomit Sengupta, Timothy R. Peterson, M. Laplante, Stephanie E. Oh, David M. Sabatini. Nature, 2010

642 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/52436db2504183bf3f7c7a74948ac9c860abd21b

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Citations in the corpus

Regulation of mTORC1 and its impact on gene expression at a glance (2013, background): “As discussed above, mTORC1 impairs PPARa activity and the expression of genes regulating lipid oxidation in the liver (Sengupta et al., 2010), whereas opposing effects have been observed in the heart and in skeletal muscles (Romanino et al.”
Akt stimulates hepatic SREBP1c and lipogenesis through parallel mTORC1-dependent and independent pathways (2011, positive): “This is consistent with recent findings that mTORC1 signaling decreases the expression of b-oxidation genes in the liver (Sengupta et al., 2010).”
Fasting: Molecular Mechanisms and Clinical Applications (2014, background): “Additional effects of fasting in human cells that can be considered as potentially ‘‘antiaging’’ are inhibition the mTOR pathway, stimulation of autophagy, and ketogenesis (Harvie et al., 2011; Sengupta et al., 2010).”
Rapamycin passes the torch: a new generation of mTOR inhibitors (2011, background): “In mice, results from organ-specific knockouts of TOR complex components in metabolically significant organs such as live”
Association between insulin resistance and the development of cardiovascular disease (2018, background): “The ketogenic diet effect can be mediated by suppressing longevityrelated insulin signaling and mTOR pathway, and activation of peroxisome proliferator activated receptor α (PPARα), the master regulator that switches on genes involved in ketogenesis [169].”
mTOR signaling in growth control and disease (2012, positive): “mTORC1 controls the hepatic production of the ketone bodies that peripheral tissues use as energy sources during fasting (Sengupta et al., 2010).”
Multi-dimensional roles of ketone bodies in fuel metabolism, signaling, and therapeutics (2017, background): “…indicates that mTORC1 suppresses ketogenesis in a manner that may be downstream of insulin signaling (Kucejova et al., 2016), which is concordant with the observations that mTORC1 inhibits PPARa-mediated Hmgcs2 induction (Sengupta et al., 2010) (also see Regulation of HMGCS2 and SCOT/OXCT1).”
Molecular mechanism of PPARα action and its impact on lipid metabolism, inflammation and fibrosis in non-alcoholic fatty liver disease. (2015, background): “Inhibition of mTORC1 and its downstream effector S6K2 during fasting promotes a cytoplasmic relocalization of NCoR1, hence increasing ketogenesis via PPARa derepression [105,106].”
Energy Metabolism in the Liver (2014, positive): “Activation of mTORC1 also inhibits PPAR α activity, β -oxidation, and ketogenesis in the fed state (240).”
mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “For example, mice with liver-specific deletion of TSC1, which have constitutively activated mTORC1 signaling, fail to generate ketone bodies during fasting due to sustained mTORC1-dependent suppression of PPARa, a transcriptional activator of ketogenic genes (Sengupta et al., 2010).”
mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “For example, mice with liver specific deletion of TSC1, which have constitutively activated mTORC1 signaling, fail to generate ketone bodies during fasting due to sustained mTORC1-dependent suppression of PPARa, a transcriptional activator of ketogenic genes (Sengupta et al., 2010).”