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This result was unexpected, but could be explained by the finding that in the absence of HSL, adipocytes undergo a compensatory decrease in the re-esterification of FA that results in decreased resynthesis of TAG and increased liberation of FA to the vasculature (144)

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756 Overexpression of ACSL4 exacerbates cerebral I/R injury in rodents, while genetic or pharmacological reduction of ACSL4 effectively prevents cerebral I/R injury

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