Hypothalamic mTOR Signaling Regulates Food Intake
By D. Cota, K. Proulx, Kathi Smith, S. Kozma, G. Thomas, S. Woods, R. Seeley. Science, 2006
1,293 citations recorded by the source corpus.
Subfields: Endocrine and Autonomic Systems, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/f37417332ae7566a5aba12c68d45ceb545bf3461
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In Endocrine and Autonomic Systems
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Citations in the corpus
- The Critical Role of Metabolic Pathways in Aging (2012, background): “Meanwhile, increased mTOR activity in the brain or activation of S6K in the hypothalamus leads to decreased appetite via modulation of leptin and ciliary neurotrophic factor (72).”
- Nutrient sensing and inflammation in metabolic diseases (2008, background): “Also, the action of mTOR in the central nervous system of rats can affect metabolism through the co-regulation of appetite and body weigh”
- mTOR: from growth signal integration to cancer, diabetes and ageing (2010, methodology): “When locally applied to the hypothalamus, Leu induced satiety through activation of mTORC1; conversely, inhibition of mTORC1 in the hypothalamus by rapamycin injection increased food intak”
- Glutamate NMDA receptor antagonists rapidly reverse behavioral and synaptic deficits caused by chronic stress exposure (2011, positive): “These doses were chosen based on previous reports demonstrating effective and selective inhibition of the respective targets (25,29).”
- A Branched-Chain Amino Acid-Related Metabolic Signature that Differentiates Obese and Lean Humans and Contributes to Insulin Resistance (2009, background): “In the first, intracerebroventricular (ICV) infusion of leucine caused reduced food intake in mice (Cota et al., 2006), although the effect of dietary BCAA supplementation was not described.”
- AMPK in Health and Disease. (2009, methodology): “The mammalian AMPK domain limits were established experimentally by partial proteolysis (395), and a stable rat 1(68-163) fragment was expressed and crystallized in the presence of -cyclodextrin (an 1-4 linked heptaglucan), as had previously been performed for other starch binding domain structural ”
- mTOR signaling in growth control and disease (2012, neutral): “mTORC1 is active in the ARC and intracerebroventricular administration of leucine or leptin to rats promotes mTORC1 activity and reduces food intake in a rapamycin-sensitive fashion (Cota et al., 2006) (Figure 4A).”
- Mechanisms of leptin action and leptin resistance. (2008, background): “LRb stimulation mediates the tyrosine phosphorylation of IRS proteins and regulates the PI 3′-kinase pathway (74– 76) as well as the AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) pathways (77, 78), although the molecular mechanisms by which LRb regulates these pathways”
- Kisspeptins and reproduction: physiological roles and regulatory mechanisms. (2012, background): “, AMPK inactivates mTOR in different cell systems (184, 478), these two metabolic cell sensors have been proposed to reciprocally cooperate in the central control of energy homeostasis (75).”
- Obesity and Leptin Resistance: Distinguishing Cause from Effect (2010, background): “, PI3 kinase is strongly activated by insulin, and mTOR is controlled by amino acid availability), and may be mediated trans-synaptically, which confounds their use as readouts of cellular leptin signaling (71,75).”