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• W2019080454 startingPage "41391" @default.
• W2019080454 abstract "Endotoxin is a potent inducer of systemic inflammatory responses in human and rodents. Here, we show that in vivo endotoxin triggers a rapid and transient decline in ATP concentration in human peripheral blood leukocytes and murine peripheral blood leukocytes and liver, which is associated with a brief increase in expression of the autophagy indicator LC3-II. In both of these tissues, the ATP concentration reaches a nadir, and autophagy is induced between 2 and 4 h post-endotoxin infusion, and homeostasis is restored within 12 h. Mouse liver SIRT1 and AMP-activated protein kinase (AMPK) protein expression levels decline precipitously within 10 min and remain below detection levels for up to 12 h post-endotoxin administration. In marked contrast, the expression of HIF-1α is induced within 90 min and remains elevated for up to 12 h. The ATP recovery is delayed, and the increases in both HIF-1α expression and autophagy are prolonged in endotoxin-challenged SIRT1 liver knock-out mice. Resveratrol prevents the decline in ATP concentration and SIRT1 expression, as well as the increase in HIF-1α expression and autophagy in liver of endotoxin-challenged wild type mice but not in SIRT1 liver knock-out mice. These results provide novel insight into the state of both cellular bioenergetics and metabolic networks during the acute phase of systemic inflammation and suggest a role for SIRT1 in acute metabolic decline, as well as the restoration of metabolic homeostasis during an inflammatory challenge." @default.
• W2019080454 created "2016-06-24" @default.
• W2019080454 creator A5013771208 @default.
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• W2019080454 creator A5048014973 @default.
• W2019080454 creator A5080821946 @default.
• W2019080454 date "2010-12-01" @default.
• W2019080454 modified "2023-09-29" @default.
• W2019080454 title "Roles of SIRT1 in the Acute and Restorative Phases following Induction of Inflammation" @default.
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• W2019080454 doi "https://doi.org/10.1074/jbc.m110.174482" @default.
• W2019080454 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3009865" @default.
• W2019080454 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20966076" @default.
• W2019080454 hasPublicationYear "2010" @default.
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