2012
DOI: 10.1126/science.1215135
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Abstract: Rapamycin, an inhibitor of mechanistic target of rapamycin complex 1 (mTORC1), extends the lifespans of yeast, flies, and mice. Calorie restriction, which increases lifespan and insulin sensitivity, is proposed to function by inhibition of mTORC1, yet paradoxically, chronic administration of rapamycin substantially impairs glucose tolerance and insulin action. We demonstrate that rapamycin disrupted a second mTOR complex, mTORC2, in vivo and that mTORC2 was required for the insulin-mediated suppression of hepa… Show more

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Cited by 1,010 publications
(993 citation statements)
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“…1C). As we previously reported (Lamming et al ., 2012), daily treatment with 2 mg/kg rapamycin efficiently inhibited the phosphorylation of both S6 S240/244, a readout of mTORC1 signaling, and AKT S473, an mTORC2 substrate. Rapamycin was equally efficacious in inhibiting phosphorylation of S6 in mice treated daily with rapamycin as in mice treated weekly (1×/7d) and sacrificed on the day following treatment (D1).…”
Section: Resultsmentioning
confidence: 94%
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“…1C). As we previously reported (Lamming et al ., 2012), daily treatment with 2 mg/kg rapamycin efficiently inhibited the phosphorylation of both S6 S240/244, a readout of mTORC1 signaling, and AKT S473, an mTORC2 substrate. Rapamycin was equally efficacious in inhibiting phosphorylation of S6 in mice treated daily with rapamycin as in mice treated weekly (1×/7d) and sacrificed on the day following treatment (D1).…”
Section: Resultsmentioning
confidence: 94%
“…2A). One treatment cycle later, we performed a pyruvate tolerance test (PTT); pyruvate can be utilized as a substrate for gluconeogenesis by the liver, permitting us to assess hepatic gluconeogenesis (Houde et al ., 2010; Lamming et al ., 2012). As expected, daily rapamycin treatment induced significant pyruvate intolerance (Fig.…”
Section: Resultsmentioning
confidence: 99%
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